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Exam 2 Flashcards

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1
Q

Chlamydia

A

Small
Gram Negative
No peptidoglycan in cell wall

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2
Q

Chlamdydia is what type of bacteria

A

Obligate intracellular bacteria

Rely on host for amino acids

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3
Q

Biphasic life cycle of Chlamydia

A

Elementary bodies

Reticulate bodies

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4
Q

Elementary bodies of chlamydia

A

Smaller rigid cell wall

*Infectious form
Extracellular survival

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5
Q

Reticulate bodies of chlamydia

A

Larger fragile metabolically active
Intracellular growth

*Replicative form

Retic=replicative

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6
Q

Different biovars of chlamydia trachoma this have different

A

Tropisms and cause different diseases

Respiratory, urgoentifcal, colorectal, conjunctiva etc.

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7
Q

Life cycle of C. Trachomatis

A

Attachment and enter of elementary body to target cells

Attaches and induces endocytosis (TARP)

Formation of Reticulate body
-using stored ATP and EB converts to replica time RB

Binary fission of Reticulate bodies
-inhibits Lysomal fusion in host cell
—forms its own membrane bound vehicle…inclusion where replication takes place

Once a threshold of RBs is reached they convert back to EB

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8
Q

TARP

A

Translocated actin recruiting protein

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9
Q

CPAF

A

Chlamydia pro teases like activity factor

-regulates cellular apoptosis signals

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10
Q

C. Trachomatis Epidemiology

A

Humans are the sole reservoir

Disease in conjunctiva or genital tract

Most common bacterial STI worldwide

Neonatal conjunctivitis

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11
Q

What is a common cause of neonatal conjunctivitus

A

C. Trachomatis

Contact with infected cervical secretions—vaginal delivery

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12
Q

Chronic follicular conjunctivitis

A

7-9 million people

Usually contracted in infancy or early childhood from mother or close contacts

Spreads directly by contact with infected secretions

  • fomites
  • fingers
  • flies
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13
Q

Chlamydia urethral infections

A

5% general population

Very contagions

Asymptotic infection in men

2-6 week incubation period **

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14
Q

Chlamydiae Tissue Tropism

A

Columnar epithelial cells of the endocervix and upper genital tract of women and the

  • urethra
  • rectum
  • conjunctiva of both sexes
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15
Q

Other tissue tropism of chlamydiae

A

Depending on biovar other cell types can also be infected

Endothelium
Smooth Muscle
Lymphocytes
Macrophages

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16
Q

MOMP

A

Initial attachment mediated by MOMP

Major outer membrane protein followed by endocytosis

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17
Q

LGV biovars

A

Can also enter through breaks in skin or mucosa

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18
Q

Once replciative cycle of chlamydia is established primary injury is due to

A

Inflammation

IL-8 released by infected epithelial cells

Leads to early tissue invasion by PMN followed by lymphocytes macrophages plasma cells and eosinophils

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19
Q

Chlamydiae LPS

A

Likely also contributes to inflammation

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20
Q

Failure of immune system to control chlamydia infection

A

Aggregate of lymphocytes and macrophages form in submucosa- leading to necrosis; fibrosis and scarring

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21
Q

Chlamydia fibrosis and scaring results in

A

Infertility in female

Blindness in the eye

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22
Q

Immunity to Chlamydia

A

Immunity takes a long time to develop and is incomplete

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23
Q

Th1r Response (chlamydia)

A

Cd4+ TCell response

TH2 direct at MOMP May participate but antibody is associated with injury in chronic forms of the disease trachoma

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24
Q

Chlamydia Trachoma

A

Chronic inflammation of eyelids can lead to scarring of cornea

  • usually seen in less developed countries
  • Often lead to blindness
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25
Inclusion conjunctivitis (Chlamydia)
Acute infection presents in newborns as mucopurulent eye discharge Mother—>infant Not associated with chonociity or blindness Can lead to infant pneumonia syndrome
26
Genial Infections Chlamydia trachomatis | Men
Similar to N. Gonorrhoeae Urethritis and epididymitis in men
27
Genial Infections Chlamydia trachomatis | Women
Cervicitis Salpingitits Urethral syndrome Can lead to pelvic inflammatory disease
28
Lymphogranuloma Venereum
LGV Caused by invasion biovars L1 L2 L3 Entry: through break in skins, transient genital lesion Results in swollen glands in groins Can also cause hemorrhagic ulcerative proctitis
29
Nucelic Acid amplification test
Used to detect chlamydia and N gonorrhoeae DNA Rapid specific sensitive
30
C trachomatis treatment
Azithromycin Doxycycline for LGV
31
Rickettsiae
Small Gram negative Nonmotile
32
Rickettsiae type of parasite
Obligate intracellular parasites
33
Reickttsiae cell envelope
LPS and two other large abundant outer membrane protein Cell wall made of peptidoglycan
34
Reickttsiae Replcaition and Growth
Obligate intracellular parasite Reductive evolution lead to loss of many core metabolic capabilities dependence on host -requires host co-factors, amino acids, Phosphorylation sugars and ATP Metabolize host derived glutamate vine aerobic respiration and TCA cycle Slow growing dividing by binary fission in host cytoplasm or nucleus
35
Reickttsiae enter host cell through
Endocytosis attachment of OMP to many cell types - induces phagocytosis - escape phagosome using phospholipase - grows freely in host cell cytoplasm
36
Reickttsiae transmitted via
Salivary gland of infected ticks or other vectors Bacteria spread locally creating necrotic Escher (black sore)
37
Tropism for vascular endothelium multiplying in endothelial cells lining small blood vessels
Results in : -Vasculitis -Vascular lesions-> hypovolemia and hypotension
38
Reickttsiae causes thrombosis
Caused by focal areas of endothelial proliferation and perivascular infiltration Leakage of red blood cells leads to rash and petechial lesions
39
Reickttsiosis two categories
Spotted Fever Group Typhus group Both characterized by fever, headache, myalgia and rash Both can be fatal due to severe vascular collapse
40
Spotted Fever Group (SFG)
Most common in US Rocky Mountain spotted fever
41
Rocky Mountain spotted fever caused by
rickettsia rickettsii Primarily a parasite of ticks Western States-Wood Tick Eastern States-Dog ticks Southwest and Midwest-lone star tick Ubiquitous-brown dog ticks
42
Adult Female Ticks
Transmit the disease Need blood meal to lay eggs Adult ticks can survive up to 4 years without blood meal
43
RMSF Clinical Aspects
6-7 days after bite ``` Fever Headache Rash Toxicity Mental confusion Myalgia ```
44
RMSF Complication
Can lead to death Blood clots (intravscualr coagulations) Low platelets (thrombocytopenia) Encephalitis (brain inflammation) Vascular Collapse Renal and heart failure
45
Rickettsia diagnosis
Serological diagnosis
46
rickettsia Treatmnet
Doxycycline Sulfonamides
47
Typhus Group
More common in Europe Causes three different Diseases
48
Epidemic Typhus Fever
R. Prowazekki, spread by body lice (Not typhoid fever) Only epidemic rickettsial disease
49
Endemic Typhus
R. Typhi Spread by rat fleas
50
Scrub Typhus
Orienting tsutsugmaushi Spread by chiggers
51
Typhus Fever pathogenesis
Human body louse gets infected during feeding R. Prowazekii are present in lice poop 5 to 10 days after infection Louse poop while they feed - bacteria enters bloodstream when human scratches bite - Louse feces are also infectious through mucous membranes of eyes and respiratory tract
52
Epidemic Typhus Symptoms
Incubation period is 1-2 weeks Rash starts on trunk Headache Malaise Myalgia
53
Epidemic Typhus Diagnosis
Serology is used to confirm but clinical history is used to justify treatment
54
Epidemic typhus treatment
Treatment must be started immediately to prevent complications Doxycycline
55
Epidemic Typhus Prevention
Louse control is best means of prevention No vaccine available
56
Endemic Murine Typhus
Resembles typhus but less severe R. Typhi Transmitted by rat Flea
57
Scrub typhus
Orient is tsutsugamushi transmitted by rodent mite larvae—Chiggers Necrotic Escher at bite
58
Scrub Typhus Symtpoms
Fever slowly increases Maculopapular rash Treatment: Docycycline
59
Bartonella
Closely related to Brucella Gram Neg Coccobacili Facultative Intracellular Parasites
60
Bartonella Primary niche
Endothelial cells Released into blood stream
61
Bartonella infects
Erythrocytes Multiply and persist until taken up by arthropod
62
bartonella Vectors
``` Ticks Fleas Sand flies Mosquitos -Can cause co infections with Lyme disease ```
63
Bartonella henselae
Cat scratch Disease
64
Cat Scratch Disease
25,000 per year Spread by cats scratch, bite, or cat fleas Flea control can prevent. Cats are carriers ``` Swollen lymph nodes Skin rash Conjunctivitis Encephalitis Prolonged fever ```
65
Bartonella Quintana
Trench Fever
66
Trench Fever
Affects homeless alcoholic men Spread by body louse Sudden onset of chills Headache Relapsing fever Maculopualr rash
67
Arthropod Disease Summary
B henselae B Quintana R typhi R proqazekii R rickettsii
68
Spirochete medically important genera
Treponema Leptopira Borrelia
69
Spirochetes
Loose Coils to rigid corkscrew Rotation and flexion for movement
70
Spirochetes wall and membrane
Flexible peptidogluycan cell wall surrounded by axial fibrils Outer bi-layered membrane (similar to gram neg)
71
ANUG
Acute necrotizing ulcerative gingivitis
72
Trench Mouth (ANUG)
Opportunistic infection - severe malnutrition - neglect of basic hygiene - immunocompromised
73
Trench mouth symptoms
``` Bleeding gums Bad breath Metallic taste Sudden onset Unbearably painful ```
74
Treponema pallidum
Highly Motile Corkscrew shaped No LPS Easily killed-drying, heat, detergents, and disinfectants
75
Treponema pallidum causes
Syphilis
76
T Pallidum relies on
Host for basic nutrients and metabolites -Minimalist pathogen Lacks energy generation pathways-no TCA or Electron Transport Chain Slow growing and no enzymes
77
Syphilis epidemiology
Exclusively human pathogen Primary or secondary lesion Tertiary syphilis is not contagious
78
Spirochetes reach ____ tissues
Subepithelial Entry unapparetn breaks in the skin or through mucous membrane Multiplies slowly in the submucosa Spreads to bloodstream
79
Primary lesion is an endarteritis T pallidum
Inflammation of inner lining of an artery and a necrotic ulceration later forms
80
Primary Syphillis
3 to 90 days after exposure Primary lesion (chancre) appears at point of contact
81
Secondary syphilis
Occurs in about 1/3 of patients Commonly involve skin mucous membranes and lymph nodes Symmetrical reddish pink non itchy rash palms and soles
82
Latent Syphilis
Following secondary syphilis No clinical symptoms Occasional secondary replace can occur Transmission to fetus is possibly during latency
83
Tertiary Syphilis
Untreated secondary syphilis develops into tertiary Can manifest in numerous ways-nervous system and cardiovascular system are the worst
84
Neurosyphilis
Invasion of nervous system headache altered behavior loss of coordination paralysis tabes dorsal is sensory deficits and dementia
85
Ocular syphilis
Can involve almost any eye structure vision changes decreased visual acuity and permanent blindness
86
Cardiovascular syphilis
Aortiits leading to aneurysms
87
Gumma
Localized granulmaotus reaction to t pallidum | May be found in skin bone joints or other organs
88
Borrelia burgdorferi
Long slender spirochetes Causes Lyme’s disease
89
Borrelia burgdorferi membrane
Outer membrane lacks LPS
90
Borrelia burgdorferi multiple classes of OMPs
Undergo antigenic variation referred to as outer surface proteins OspA and AspC differentials expressed deepening on state of tick or mammalian infection
91
Lyme Disease primary reservoir
Rodents are primary -tick larvae feed on mice and acquire Borrelia burgdorferi Lyme disease is mainly contracted in spring or summer
92
Enzootic cylce of Borrelia burgdorferi
Two years and involves 3 blood meals Larvae hatch from uninflected eggs Feed on infected animal host acquire Borrelia burgdorferi After a period of dormancy infected larvae molt into nymphs, which feed and transmit Borrelia burgdorferi to vertebrate host Nymphs molt into adults which feed on an animal and mate Only found where deer are present
93
Primary Lyme Diseae
Symptoms can begin within the first month after tick bite Bull’s eye pattern-macula or pauper rash appears at bit site Fever fatigue myalgia headache joints pions and mild neck stiffness
94
Lyme disease secondary
Secondary stage may develop days to months after primary rash- nervous system and CA system involvement Fluctuating meningitis, cranial nerve palsies AV block Joint arthritis Chronic lymes diseases
95
Treatment of Borrelia burgdorferi
Doxycycline and B lactams Response to antibiotics is slow
96
Legionella pneumophila
Gram negative Aerobic Small bacilli Water our and found in soil Facultative intracellular bacteria
97
Legionella pneumophila type of pathogen
Opportunistic pathogen-only affects smokers and immunocompromised hosts impaired in cell mediated immunity Facultative intracellular bacteria-requires special media to isolate
98
Legionella pneumophila causes
Atypical pneumonia
99
Legionella pneumophila virulence factors
``` Pili Flagella LPS Type IV secretion systems Legionella contains vacuole Low metabolic state ```
100
Legionella pathogenesis
Facultative intracellular bacteria -can multiply inside free living amoebas other Protozoa and alveolar macrophages
101
Legionella Infection
Infection starts when aerosolized droplets of contaiminated water are breathed in to the lungs Begins growing in macrophages causing inflammation producing necrotizing multifocal pneumonia
102
Legionella Containing Vaculoue
Effector proteins interfere with cell trafficking | -once inside bacteria surround themselves in a membrane bound vacuole-fusion with lysosomes is blocked
103
Intracellular multiplication of Legionella pneumophila
Is key to l pneumophila virulence Innate and adaptive mechanisms are important to clear the infection and slow down bacterial replication
104
_____ in ____ and dendritic cells recognize legionella LPS
TLRs Macrophages
105
TH1 adaptive immune response
INF-gamma IL2 and IL18 are produced and activated macrophages and intracellular killing of legionella -cell mediated immunity is important
106
Legionellosis are linked to
Large complex man made water systems found in: Hotels Hospitals Nursing Homes Cruise ships
107
Two forms of legionellosis
Legionnnaries disease Pontiac Fever Both spread by contaminated water droplets
108
Legionannaires Disease
Severe form of the disease pneumonia
109
Pontiac Fever
Milder self limited form of disease with flu like symptoms No pneumonia Can also spread by exposure to contaminated soil
110
Symptoms of Legionnaires Disease
Starts with myalgia and headache rapidly rising high fever Dry cough on second or third day and chest pain Chills vomiting diarrhea confusion and delirium Hepatic dysfunction also common
111
Diagnosis of Legionella pneumophila
Direct fluorescent antibody with culture Gram stain fails Can be cultured on special media
112
Legionella pneumophila Treatment
Fluoroquinolong or azithromycin are current preferred treatments Erythromcyin penciling doesn’t work-produce beta lactamases
113
Prevention of Legionnaires
Minimize aerosols in public places from contaminated water Prevention is complicated by legionella bacteria are relatively resistant to chlorine and heat so hard to prevent contamination -forms biofilm
114
Zoonoses
Infections in humans acquired by direct or indirect contact with animals
115
Coxiella burnetii
Q fever -inhalation of soil or dust contaminated with after birth or infect animals
116
Yersina pestis
Bubonic plaque | Exposure to fleas from infected rodents
117
Brucella
Undulant fever Direct contact with infected animals Ingested of contaimnated dairy products
118
Fancisella
Tularemia Direct contact with infected mammal Inhalation Bite of infected tick
119
Pasteurella multocida
Soft tissue infection | -cat or dog bite
120
Coxiella
New bacterial species closely related to legionella
121
Coxiella burnetii
Gram negative Small coccobacilli Causes Q-fever Low infectious dose Soil and animal sources
122
Coxiella burnetii type of pathogen
Obligate intracellular pathogen -prefers macrophages and phagocytic cells Preferred port of entry in lung
123
Coxiella Virulence Factors
LPS Type IV secretion system Resistant to low pH and enzyme of phagolysomes CCV-coxiella contains vacuole Biphasic life cycle
124
CCV
Coxiella contains vacuole Phagolysome like compartment where coxiella replicates
125
Biphasic life cycle
Small cell variants | Large cell variant
126
Small cell variants
Not metabolically active Like a spore is restart to environmental
127
Large cell variant
Metabolically active form After invasion of host cells coxiella swtiches from SCV to LCV
128
Coxiella pathogenesis
Aerosol transmission -inhaled into lungs Binds to alveolar macrophages and is passively taken up through phagocytosis Affinity for reticuloendothelial system Can also invade non phagocytic cells
129
Intracellular trafficking of coxiella burnetii
Once in a phagosome-lysomal fusion occurs The coxiella expands the compartment size creating a CCV transition to the metabolically active LCV and begins to replicate-takes 6 days
130
Clinical features of Q fever
Symptoms begin 20 days after inhalation Flu like symptoms Nonproductive cough Abnormal liver function
131
Q fever treatment
Most people recover without antibiotics 2 weeks with doxycycline
132
Sylvatic cycle
Fleas leave an infected rodent and pass the infection to other in the population. Rarely transmits disease to humans
133
Urban Cycle
Masses of rats in close contact with humans, infected with fleas that bite humans and transmit the infection to many
134
Pneumonic plaque
Results when humans infected with Y. Pestis develop bacteremia where it can infect the lungs leading to person to person spread
135
Yersinia pestis
Gram negative Bacillus Nonmotile
136
Virulence factors of Y. Pestis
Phospholipase D resist antibacterial factors in flea gut Starves fleas making them constantly vomit bacteria into wound. Coagulase and polysaccharide biofilm
137
Yops (y pestis)
Two types of proteins 1 destroy host cells 2 disrupt host cells
138
Y Pestis one inside professional phagocytes effector
yops disrupt host cells
139
Eventually y pestis enter bloodstream
Reach regional lymph node and produce bubo
140
Bubo
Hemorrhagic suppurative lymphadenitis Bacteremia—> toxic shock-LPS endotoxin, yops, protease and extracellular products
141
Y pestis (palgue) diagnosis
Gram stained smears of aspirates from bubo show bipolar staining gram negative bacilli
142
Y pestis treatment
Gentamicin or streptomycin
143
Brucella abortus
Gram negative rods Non motile Aerobes -cannot ferment carbohydrates Slow growing
144
Brucella abortus unusual envelope
Phosphatidyucholine resembles eukaryotic cells
145
Brucellosis
Chronic infection persist for life Reproductive organs: infects mammary glands, uterus placenta, seminal vehicle, and epididymis Causes abortion, sterility and decreased milk production in cattle goats and hogs
146
Brucellosis is spread
By direct connect with infected tissues and ingestion of contaiminated feed
147
Systematic control
Of brucellosis is effective at preventing infections - vaccination of animals - eradication of infected animals
148
Brucella Type of parasite
Faculatative intracelluar parasite of epithelial cells and phagocytes
149
Brucella once past skin or mucous membrane barrier
Able to evade innate immunity-specifically TLRs | -outer membrane lipids resemble eukaryotes
150
Brucella multiply in mar crop hates in
The liver sinusoids spleen bone marrow and reticuloendothelial system -forming granulomas
151
Brucella intracellular survival is
Depending on inhibition of phagosome lysome fusion and apoptosis of host cell Type IV secretion system similarly to legionella
152
Brucella in placenta
In cows presence of erythritol stimulate growth Humans don’t have it. Can’t infect placenta
153
Brucella Immunity
Antibodies are formed but likely not protective T cell mediated immune response is critical to control of disease Th1 responses with cytokines associated with clearing of Brucella from macrophages
154
Symptoms of Brucellosis
7 to 21 days after infection Periodic drenching night sweats (undulant fever) Enlarged lymph noddes Splenomegaly is most common
155
Brucella diagnosis
Doxyclcine in com one with rifampin No vaccine for humans Slow growth requires long incubation periods
156
Francisella tularnesis
Gram negative Non motile Aerobic Causes rabbit fever tularemia
157
Francisella tularensis type of parasite
Faculatative intracellular parasite | Aerobic and requires cysteine for growth
158
Francisella tularensis Tier
Tier 1 Low infectious dose Ease of spread High virulence
159
Francisella tularensis Virulence factors
Lipid rich capsule Unusual LPS Natural infection confer long lasting immunity -antibody tigers remain high for many years
160
Francisella tularensis LPS
Doesn’t stimulate innate immunity (unusual) BUT LPS does induce protective antibodies
161
Tularemia spread by
Contact with an infected mammal or blood feeding arthropod Rabbits squirrels can be infected without any symptoms Low infectious dose Not found in British isles Africa South America or Australia 100-200 cases per year
162
Francisella tularensis minor routes of infection
Minor skin abrasion Inhalation
163
Francisella tularensis LPS is
Not recognized by innate immune system (TLR)
164
Tularemia lesion
Often develops at site of infection and becomes ulcerated
165
Tularemia after macrophage ingestion
Resides in opahgosome Resist lysome fusion and escapes to host cytoplasm
166
Francisella tularensis can multiple in many cell types
Hepactocytes kinda alveolar epithelial cells Infects reticuloendothelial organs often forming granulomas
167
Granulomas
Type of inflammation Collection of immune cells -macrophages Occurs when the body attempts to wall off a foreign substance that it cant eliminate
168
Tularemia-clinical aspects
Incubation period 2 to 5 days Disease progression depends on site of inoculation and extent of spread All cases begin with acute onset of high fever
169
Tularemia disease depends on site of inoculations
``` Ulceroglandular form Oculoglandular form Oropharyngeal form Pneumonic form Typhoid also form ```
170
Ulceroglandular form of tularemia
Most common Tick bite or handling infected animal Ulcer forms and swollen lymph nodes
171
Pneumonic form tularemia
Most serious form Inhalation of contaiminated dust or aerosols restyle in pneumonic tularemia or infection similarly to typhoidal form tularemic pneymonica can also develop through bacteremia
172
Typhoidal form of tularemia
Combination of the general symptoms without locating symptoms of other syndromes
173
tularemia treatment
Treatable with antibiotics Live attenuated vaccine is available for high risk populations
174
Pasteurella multocida
Gram negative Susceptible to penicillin unlike most gram negative rods Normal respiratory flora of many dogs and cats
175
Pasteurella multocida Type of parasite
Facultative anaerobes Oxidase positive ferements a variety of carbohydrates
176
Pasteurella multocida common causes
Most common is dog/cat bite or scratch Soft tissue infection usually develops within 24 hours of animal bite or scratch Diffuse cellulitis with a well defined erythematous border
177
Vibrio Cholerae pH and why
Preferred pH 8-9.5 produces cholera toxins
178
2 main biotypes can cause cholera
Classical El Tor
179
Vibrio cholerae can produce what in the environment
Biofilm
180
V. Cholerae virulence factors
Flagella | Pili to adhere to mucosal tissue
181
V cholerae pili
Allow to adhere to mucosal tissue Shift from saltwater to reduced ion levels found in body leads to expression of pili and to the toxin Main regulator of pathogenicity island and ToxR
182
Cholera toxin
Phage encoded
183
Cholera toxin leads to
Excessive accumulation of cAMP This causes hypersecretion of Cl K Bicarbonate
184
Cholera is spread
By contaminated water Humans can spread the disease
185
Cholerae incubation period
2 days
186
______inoculum is needed to cause disease
High Only 01 and 0139 can cause disease
187
Effect of cholera toxin
Can lose many liters a day -no WBC/RBC Fluid contains a significant amount of K and Bicarbone which can lead to hypokemia and metabolic acidosis
188
Enterotoxigneic Coli is the leading
Cause of morbidity and mortality in children under 2 Also travelers diarrhea
189
E. Coli transmitted by
Contaminated food and water
190
E. Coli colozines what
Proximal small intestine Must adhere to cause disease
191
Enterotoxigenic Coli adherence factors
Colonizing factor CF pili
192
E. Coli 2 toxins
Heat label toxin Heat stable toxin
193
Heat labile toxin (E. Coli)
A-B toxin in an enterocyte it leads to secretion of chloride ions, blockade of NaCl reabsorption
194
Heat stable toxin (ST) (E. Coli)
Binds to cell leading to signaling cascade that ends with fluid and electrolyte secretion
195
E. Coli Immunity
Let and CF specific SLgA No inflammation
196
How to rule of vibrio cholerae for diarrhea
Have eaten shellfish or been to an endemic area Thiosulfat citrate bile sucrose agar Agglutination test (el tor strain) Serological testing Inoculate plates with diluted stool samples Not very Reich medium so fastidious G wont grow Aerobic incubation kills the anaerobes
197
Treatment for secondary diarrhea agents
Oral rehydration -mix of sugar and salt Antibiotics can help shorten duration or reduce severity
198
Secretory diarrhea antibiotics
Tetracyclines for vibrio infections-doxycycline 2nd generations fluorquionolones for ETEC- ciprofloxacin
199
E. Coli and V. Cholerae
``` Small intestine Copious amounts of watery stool No blood in stool No leukocytes in stool No tissue damage ```
200
Invasive Bacterial Pathogens (salmonella, shigella)
``` Large intestine Small volume of stool Bloody stool Leukocytes in stool Tissue ulcerations ```
201
Enterohemorrhagic e. Coli and Enteropathogenic E. coli
Lower small intestine/Upper large intestine Colonization causes attaching and effecting lesion Blood in stool and possibly urine
202
Urinary Tract Infections
UTIs are the most common form of bacterial infection of an organ system (not including the mouth) and the most frequent cause of doctors vistas by adaults
203
Cystitis
Inflammation in the bladder
204
Uncomplicated UTI
All normal defense mechanisms are intact No recent hospital admissions Disease limited to lower urinary tract Usually UPEC or other commensalism E. Coli
205
Complicated UTI
Some structural abnormality in urinary tract Recently admitted to hospital Disease mot likely will spread to kidneys Usually other Enterobacteriacea
206
Natural defenses found in urinary tract
``` Complete voidance of bladder peristalsis Ureterovescile valves Mucous layer PH ```
207
Pyelonephritis (kidney infection)
Cystitis can spread to the kidney via retrograde flow from the bladder to the kidneys - neurologic disorders - uterovescile valves not fully formed in kids - Pregnancy hormones Urethral catheters Urinary tract stones
208
UPEC - Uropathogenic E. Coli
Type 1 Pili P Pili are needed for ascending infections Can invade superficial epithelial cells Alpha hemolysin and cytotoxic necrotizing factor cause injury
209
Additional cause of uncomplicated UTI
Proteus mirabilis
210
Proteus mirabilis
Occurs in uncomplicated and nosocomial infection, abnormal urinary tract structure more likely to have UTI caused by P. Mirabilis
211
Which UTI is more severe P mirabilis or E. Coli induced
P mirabilis
212
P. Mirabilis virulence factors
Flagella An adhesion on the fimbriae is specific for urinary epithelium Hemolysins IgA protease Urease an enzyme that readies the pH of urine
213
Proteus mirabilis urease
An enzyme that raises the pH of urine Urea—> 2 NH3 + CO2 Bacteria will grow better in the less acidic environment Toxic to renal cells Enhances formation of struvite urianry stones which can lead to a chronic infection
214
UTI Diagnosis
Surprisingly difficult to positively ID the causative agent of a UTI Count bacteria in the urine Proteus can be diagnosed by alkaline urine and urease
215
Dysuria
Painful urination
216
Pyuria
WBC/pus in urine
217
UTI treatment
Variety of antimicrobials TMP/SMX first choice
218
Klebsiella
Nonmotile, pili aid in adherence Capsule contributes to growth phenotype of large mucous colonies Usually infect the respiratory and urinary epithelium
219
Type 1 Pili (klebsiella)
Important for adherence to urinary tract epithelial cells
220
Type 3 pili (klebsiella)
Important for adherence to respiratory tract epithelial cells
221
Klebsiella enterotoxin is similar to ___ and ___
ST LT So they can induce secretory diarrhea
222
Aerobactin
An iron sequestering protein
223
Primary klebsiella virulence factor
Antiphagocytic capsule
224
K. Pneumonia type 258
Infamous for being multi drug resistant Implicated in hospital acquired respiratory urinary tract and blood stream infection
225
helicobacter pylori Type of pathogen
Microaerophilic slow growth
226
helicobacter pylori can colonize what
The stomach
227
helicobacter pylori secretes
Urease | -raises the pH
228
Vacuolating cytotoxin (helicobacter pylori)
Can cause apoptosis of host cells
229
helicobacter pylori mode of transmission
Unknown but likely fecal-oral or even oral-oral route
230
helicobacter pylori identified as a __
Class I Carcinogen
231
helicobacter pylori Cag+ can lead to
The development of gastric adenocarcinoma or gastric mucosa associated lymphoid tissue lymphoma
232
Type IV secretion system (helicobacter pylori)
Injects VacA and Cag into gastric epithelial cells
233
H. Pylori uses flagella to
Propel itself into the mucus layer where it secretes even more urease.
234
Outer membrane proteins of H. Pylori are used to
Adhere to gastric epithelial cells
235
helicobacter pylori causes inflammation which results in
Epithelial cell death and ulcer formation
236
helicobacter pylori inflammatory effector molecules cause epithelial to produce _______
IL-8
237
helicobacter pylori downregulation of somatostatin producing
D-cells
238
H pylori infection can lead to many different diseases
Peptic ulcer disease Chronic superficial gastritis Lymphoproliferative disease Chronic strophic gastritis —>adenocarcinoma
239
helicobacter pylori primary infection can be
Silent or can lead to nausea/upper abdominal pain Can also cause non-specific symptoms such as belching , heartburn, dysphasia, globes sensation
240
Diagnosis of H. Pylori
Urea breath test
241
Urea Breath Test
Patient ingests a labeled urea. Urease in stomach can break it down into a labeled CO2 that can be exhaled and quantified
242
H. pylori treatment
2 lines of treatment with many side effects
243
H. Pylori First line of treatment
Proton pump inhibitor Antibiotic cocktail -usually clarithromycin and metronidazole or amoxicillin
244
H. Pylori second line of treatment
Proton pump inhibitor Bismuth subsalicylate Tetracycline 500 mg Metronidazole 500 mg
245
What is a mucosal surface
Surface that interacts with air that has associated glands for secreting mucus
246
Defense of mucosal surfaces
Innate immunity Adaptive immunity No specific barrier defenses
247
Transmission of gram-Negative mucosal pathogens
Feces to mouth via any of the seven Fs ``` Feces Food Fluids Fingers Flies Fomites Fortification ```
248
Natural barrier Defenses of GI tract
Acidity Motility Mucous layer and underlying glycocalyx Tight junctions
249
Lysozyme (muramidase)
Cleaves B 1,4-glycosidic linkages between N-acetylnuramic acid and N-acetylyglucosamine
250
Murein can be
Exposed or hidden
251
Secretory antimicrobial compounds
``` Lysozyme Lactoferrin Cathelicidin Defensins Secretory immunoglobulins ```
252
Lysozyme
Cleaves linkage between N-acetylnuramic acid and N-acetylglucosamine
253
Lactoferrin
Bacteriostataic effects via sequestering iron
254
Cathelicidin
Disrupts bacterial membranes of Gm- and Gm+ as well as fungi
255
Defensins
Creates pores in microbes Alpha defensins produced by neutrophils and paneth cells (in intestines) B defensins produced by epithelial cells
256
How do pathogenic bacteria overcome these innate barrier defenses
Acid resistance Fimbriae/pili Bacterial structures
257
Acid resistance
Microbes with low infectious dose to tend to be acid resistant Shigella Enteroinvasisve E. Coli
258
Fimbriae/Pili (barriers of defense)
Adhere to tissue to resist being shed
259
Bacterial structures (barrier defense)
Gram-/Gram+ cell membrane sensitivities to bactericides compounds Cationic amino acids into cell membrane sensitivities to bactericidal compounds Siderophores to sequester iron in low iron environments. (E. Coli)
260
Macrophage as an important component of mucosal immunity
Macrophages recognize microbes via pattern recognition receptors. This leads to activation of the macrophages and the ability to kill many microbes
261
Activation of pattern recognition receptors also initiates
The inflammatory response
262
Enterobacteriaceae family
Gram - Nonspore forming Non acid fast rod Facultative growth ALL have endotoxin some secrete exotoxins
263
Enterobacteriaceae family Cell wall components
O antigen K antigen H antigen
264
O antigen
Outer antigen LPS
265
K antigen
Polysaccharide capsule
266
H antigen
Flagella
267
2 most common infections of enterobacteriaceae
UTIs | Acute Diarrhea
268
Escherichia coli
Most E. Coli ferment lactose and produce indole Use O, K, and H antigens to determine serotype
269
E. Coli Pili: Type 1
Most common bind D-mannose residues on epithelial cells has on/off switch
270
E. Coli Pili: P pili
Bind diglactoside found within urinary tract and some erythrocytes
271
E. Coli Pili: other
Common to diarrheal strains bind to enterocytes
272
E. Coli toxins: alpha hemolysin
Pore forming cytoxin
273
E. Coli toxins: Cytotoxic necrotizing factor
CNF A-B toxin that produces G proteins (disrupts intracellular signaling). Often made with alpha hemolysin
274
E. Coli toxins: Shiga toxin
(Stx) A-B toxin that blocks protein synthesis by ribosomal modification
275
UPEC
Uropathogenic E. Coli
276
ETEC
Enterotoxigenic E. Coli
277
EPEC
Enteropathogenic E. Coli
278
EIEC
Enteroinvasive E. Coli
279
EHEC
Enterohemorrhagic E. coli
280
EAEC
Enteroaggregative E. Coli
281
Bundle forming pili
EPEC uses to adhere to distal small intestinal enterocytes
282
Type III secretion system: EPEC
Inject over 30 E. Coli secretion proteins into host cell
283
EPEC: Intimin-Tir
Interaction leads to formation of attaching and effacing lesion
284
EHEC produces toxins that leads to
Hemolytic uremic syndrome Associated with bloody diarrhea
285
EHEC source
Animal products, unpasteurized juices, fresh vegetables
286
Most common EHEC
E. coli 0157:H7
287
EHEC primary reservoir
Cattle
288
EHEC produces
A shiga toxin - hemorrhagic colitis - hemolytic uremic syndrome
289
EHEC causes an attaching
Effacing lesion in colon via long polar fimbriae lead to A/E lesions similar to EPEC
290
Shiga toxins attack what
Mucosal surfaces are heavily vascularized, shiga toxins attack small blood vessels of the large intestines -This can be intensified when inflammatory cytokines are present
291
EIEC is similar to
Shigella and causes a disease that is milder versions of shigellosis - children under 5 - usually contaminated food/water - humans only reservoir
292
EAEC can lead to
Watery diarrhea that can last longer than 14 days Involves tight adherence to epithelial cells in a stacked brick pattern
293
Hallmarks of intestinal E. Coli infection
Symptoms usually begin a couple of days after inoculation and is self limiting Exceptions: EAEC diarrhea can last for weeks EPEC can become chronic EHEC and EIEC can have bloody diarrhea
294
E. Coli treatment
Diarrheal disease-supportive therapy, keep hydrated if needed -Hemorrhagic colitis/HUS may require hemodialysis/hemispheres is ABX can be reduced duration of diarrhea but usually not needed Antimotility agents are contraindicated, especially for EIEC and EHEC
295
Shigella is specialzied
E. Coli All species are invasive and multiple within epithelial cells
296
Shigella antigens
O and K -O antigens are main NO H antigens
297
Shigella produce
Shiga toxin
298
Shigella Species
Shigella dysenteria Shigella Flexneri Shigella Boydii Shigella Sonnei Subgroups found within each of these
299
Which shigella spp. Cause most severe disease
Shigella dysenteriae (serogroup A) Type 1
300
Shigellosis
Strictly human disease Can be spread by food/water contaminated by humans (oral/fecal) Incidence and prevalence is directly related to personal and community sanitation Wars and disasters enable outbreaks
301
Shigellosis inoculum
Very low little as little as 10 organisms | -acid resistant
302
Shigella pathogenesis
Mucosal surface is resistant to infection but basal surface is not 1) enter M cells, via outer membrane proteins called invasion plasmid antigens. Transcytose through M cell to a macrophage 2 escapes phagosome, causes apoptosis of macrophage, bacteria can now escape dead macrophage in the lamina propria 3 Type III secretion system is used to inject invasion plasmid antigens via the absolute real surface of an enterocyte (NOT an M cell) 4 Host cell cytoskeleton rearrangements occur to help internalize shigella via endocytosis 5 Shigella use host actin to move inside the host cell
303
When does an ulcer form during shigella
An ulcer develops when invaded cells die and slough off | -ulcers also allow shigella to reach the lamina propria
304
All species of shigella induce what
An inflammatory diarrhea with leukocytes in the stool S. Sonnei induces a watery stool still with leukocytes
305
Shigella dysenteriae type 1 is different
Significant mortality even in healthy individuals Produces Shiga toxin - kills intestinal epitheal and endothelial cells - Disrupts Na absorption - Toxin can be systemic
306
Shigella immunity
Infection does produce immunologic protection however there is NO CROSS PROTECTION against other serotypes
307
Shigella diagnosis
Stool culture | O antigen agglutination tests to determine serotype
308
Shigella treatment
Usually self limiting Antibiotics such as ciprofloxacin and azithromycin can help shorten the illness period
309
Salmonella infection
Fecal (human or animal)—oral transmission More acid sensitive than shigellae
310
Low pH induces the expression of what in salmonella
Expression of at least 40 proteins found on pathogenicity islands on large virulence plasmids
311
Salmonella pathogenesis (5 steps)
1 Orgnaims make contact with M cell and injects effector molecules into cell with Type III secretion system 2 These events induce surface ruffles and uptake of the organisms 3 Multiples and remains within cell vesicles for many hours 4 Organims related to lamina propria inflammatory response is activated ingested by phagocytes then kills phagocyte 5 Macs engulf most but some escape to cause a transient bacteremia —typhoid serovars will survive and grow within the macrophages
312
Salmonella Typhi
No animal reservoir Strictly human pathogen Asymptoamtic carriers Carries have colonized gall bladders and the organims can be cultured from their feces
313
Salmonella typhi survival in macrophages
Within macrophages they can live longer than other serovars due to its ability to inhibit the oxidative burst -Enters lymphatic system via macrophage Endotoxin causes fever
314
Typhoid fever Path
INgestion Small intestines Mesenteric lymph nodes Thoracic duct Multiplication in macrophages Gallbladder Bile Small intestine
315
Salmonella immunity
Humoral (Th2) and cell mediate immunity (Th1) are both activated -salmonella may be able to exploit host response to help its survival in the host
316
Salmonella diagnosis
Culture from stool or blood can aslo identify O sero group
317
Gastroenteritis treatment (salmonella)
Treatment includes fluid/electrolyte replacement -antibiotic treatmnet is reserved for severe cases as it can increase the duration of infection and the incidence of the carrier state
318
First line Typhoid fever treatment
Includes antibiotics such as ciprofloxacin
319
Corynebacterium diptheriae
Gram + Aerobic pleomorphic club shaped rod Catalase positive
320
Diptheroids inhabit
The pharynx, nasopharynx, distal urethra and skin
321
C. Diptheriae produce
Diptheriae toxin which is encoded on a lysogenic bacteriophage
322
Diptheroids
Nonpathogenic commensal corynebacterium
323
C. Diptheriae
Reside mainly in oropharynx and are pathogenic
324
Diptheria
A disease caused by the local and systemic effect of diptheria toxin The local disease is a severe pharyngitis or tonsillitis. Typically accompanied by a plaque like pseudomembrane in the throat and tracheas
325
Diptheria toxin in the blood circulation
Can affect multiple organs but the most important is the heart -the toxin produces an account myocarditis
326
Diptheria toxin
An A-B endo Toxin Toxin binds to cells via B subunit->internalize by endocytosis vacuole At low pH of vacuole toxin unfolds and A subunit translocates to cytoplasm A subunit ADP-ribosylate leads to inhibitor of protein synthesis
327
A-B toxin
Are two component protein complexes secreted by a number of pathogenic bacteria. They can be classified as type III toxins because they interfere with internal cell function
328
C. Diptheria spread
By droplet spread, by direct contact with cutaneous infections and to a lesser extent by formites
329
C. Diptheria convalescent
Some subjects become convalescent pharyngeal or nasal carries and continue to harbor the oraganism for weeks months or longer -rare where immunization is widely practiced
330
C. Diptheria diagnosis
Primary diagnosis is clinical Culture on selective medium containing potassium telluride such as Tinsdale medium
331
Diptheria toxin is antigenic
Stimulating the production of neutralizing antitoxin antibodies during natural infection
332
Formalin inactivated in diptheria
Formalin inactive toxin remains antigenic and can stimulate the production of neutralizing antibodies
333
Diptheria treatment
Early administration of diptheria antitoxin -an antiserum produced in horses Penicillins, cephalosporins, erythromycin and tetracline can be used to eliminte
334
Diptheria immunization
Immunization with diptheria toxoid provides protection against toxin by stimulating production of neutralizing antibodies - done in the first year of life with 3-4 shots - booster every 10 years
335
Listeria moncytogenes
Aerobic Gram + Rod
336
Listeria resembles what other two bacteria
Corynebacterium and streptococcus
337
How to distinguish listeria from streptococcus
Catalase positive
338
Distinguish listeria from corynebacterium
Demonstrate tumbling motility in fluid media at temperatures below 30 Celsius
339
Type of pathogen: L moncytogenes
Intracellular Only L. Monocytogenes is pathogenic to humans out of 6
340
Listeriosis
Usually does not present clinically until there is disseminated infection
341
Disseminated infection of Listeria in adults
Usually involve general manifestation such as fever malaise and occasional bacteremia -Can cause encephalitis and meningitis
342
Listeria moncytogenes in during pregnancy
May also be transmitted transplacentally to the fetus resulting in still birth or severe or sudden onset of neonatal sepsis
343
Listeria monocytogenes major virulence factors
Internalize | Lysteriolysis O
344
Listeria monocytogenes intracellular and infects
Phagocytes Internalins mediate attachment to the host cells Internalized by endocytosis
345
Listeriolysin O
Loses endocytic vacuole
346
L. Monocytogenes in cytoplasm
Replications then propels its escape from cytoplasm and infect neighboring cells by actin polymerization
347
Listeria monocytogenes
Blood and CSF culture show Beta hemolytic gram positive rods
348
Listeria monocytogenes epidemiology
Ubiquitous in nature can be found in soil water intestinal tract of animal
349
L. Monocytogenes can be difficult to elimante why
Forms biofilms
350
L. Monocytogenes food born pathogen
Spread from deli meat dairy and in cooked food stored at low temperatures
351
L. Monocytogenes immunity
Involves both innate and adaptive immune response - Neutrophil mediated killing of bacteria, innate immunity - T cell mediate immunity for resolution of infection and long term protection
352
L. Monocytogenes prevention
No vaccine Avoidance of unpasteurized dairy products and thorough cooking of animal products especially for immunocompromised individuals
353
L. Monocytogenes Treatment
Ampicillin and trimethoprim/sulfamethozaxole Ampicillin combined with gentamicin is considered the treatment of choice for fulminant cases and in patients with severe compromise of T cell function
354
Bacillus anthrasis
Gram + Aerobic Spore forming long chain rods Non motile
355
Bacillus anthrasis endospores
Are extremely hard and have been show to survive in the environment for decades
356
Bacillus anthrasis produce
Anthrax A, potent exotoxin
357
Bacillus anthrasis dwells where
In soil | Zoonotic
358
Human anthrax
Typically an ulcerative sore on an exposed part of the body which usually resolves without complications
359
Bacillus anthrasis: antiphagocytic effect
Glutamic acid capsule required for virulence
360
Bacillus anthrasis: causes edema at site of infection
Adenylate cyclase acitivty of anthrax toxin
361
If anthrax is inhaled
A fulminant pneumonia may lead to respiratory failure and death
362
Anthrax is primarily a disease of
Herbivores such as horses sheep and cattle who acquire it from spores of B anthracite contaiminating their pastures
363
Anthrax infects human
Through contact with herbivore animals or their products in a way that allows the spores to be inoculated through skin, ingested, or inhaled Biological warfare
364
Bacillus anthrasis diagnosis
Culture of skin lesions Sputum Blood And CSF are the primary anthrax diagnosis Hemolysis and motility exclude B anthracis
365
Bacillus anthrasis: Immunology
Immunity against B anthracis are not known Favors antibody directed against the toxin complex The capsular glutamic acid is immunogenicity but antibody agisnt it is not protective
366
Bacillus anthrasis: treatment
Ciprofloxacin or doxycycline Eradication of animal anthrax is most important Live and inactive vaccines are available
367
Mycoplasma pneumoniae
Is an aerobic but most other species are facultatively anaerobic
368
Mycoplasma and Ureaplasma
Smallest free living micro organims lack cell wall
369
Mycoplasma and Ureaplasma cells are bound
Only by a single trial intr membrane containing host derived or exogenous sterols
370
Mycoplasma pneumoniae
Walking pneumonia Infection involves the trachea bronchi, bronchioles and peribronchial tissue and may extend to the alveoli and alveolar walls ``` Characterized by Nonproductive cough Fever Headache Radiologic and clinical evidence of scattered areas of pneumonia ``` Pharyngitis and otitis common
371
M. Pneumoniae: CARDS toxin
Interferes with ciliary action and causes nuclear vacuolizaton and fragmentation of tracheal epithelial cells leading to inflammation and desquamation the mucosa ADP-ribosylating
372
Mycoplasma pneumoniae: Infection
Droplet spread Low infecting dose Common in teenagers
373
Mycoplasma pneumoniae : Immunology
both T and B cell mediated immune responses occur and generally appear to be effective in prevent reinfection however can occur
374
Mycoplasma pneumoniae : Nonspecific immune response
Nonspecific immune responses to glycolipids of the outer membrane of the organism can be detrimental to the host due to the cold agglutinins, IgM, hemolysis, and Raynaud phenomena
375
Mycoplasma pneumoniae : Diagnosis
too slow to culture Complement fixation is the most common PCR best hope
376
Mycoplasma pneumoniae : Treatment
Macrolides doxyclcine Fluroquinolones are effective alternatives
377
Mycoplasma pneumoniae : prevention
No vaccine
378
Mycoplasma genitalia and 2 species of ureaplasma
Leading candidates to join Neisseria gonorrhoeae and chlamydia trachomatis as causes of sexually transmitted genital infection
379
Mycobacteria
Slim poorly staining bacilli Nonmotile Obligate aerobes Do not form spores
380
Mycobacteria either live in
An animal host (pathogenic) Or Environment (nonpathogenic)
381
What makes mycobacteria unique
Lipid rich cell wall
382
M. Tuberculosis: Disease
Tuberculosis is as systemic infection manifested only by evidence of an immune response in most exposed individuals -the disease either progresses or more commonly reactive after an asymptomatic period often years
383
Symptoms of active TB
Chronic pneumonia with fever Couch Bloody sputum Weight loss Devastating when it reaches CNS
384
M. Tuberculosis: Treatment
2 lines Firs line: Isoniazid, ethambutol, rifampin, pyrazinamide ``` Second line drug: Para aminosalicyilc acid Ethionamide Cyclosporine Fluorquinolones ```
385
M. Tuberculosis: prevention
BCG vaccine Protein even against meninges tuberculoses and efficacy against pulmonary TB varies
386
M. Tuberculosis: Immunology
High innate immunity against disease TH1 immunity important Cytoxic CD8 Lymphocytes
387
M. Tuberculosis: Diagnosis
Acid fast staining PCR Tuberculin tests Qauntiferon gold
388
M. Tuberculosis: Epidemiology
1 inhaled droplets 2 multiplication in alveoli with spread through lymphatic drainage then blood 3 macrophage engulf 4 bacteria multiply in nonactivated macrophage 5 TH1 cellular immune response attempt to activate the macrophage by secreting cytokines 6 if successful disease is arrested 7 inflammatory elements of delayed type hypersensitivity are attracted and cause destruction. If activation is not successful DTH injury and disease continue
389
Deactivation tuberculosis
Deactivation typically states in the upper lobes of the lung with granulomas formation. DTH mediated destruction can form a cavity which allows the organims to be coughed up to infect another person
390
Actinomyces
Gram + Elongated rods that branch at acute angle Slow growers
391
Actinomyces type of pathogen
Microaerophilic/strictly anaerobic Commensal microbe found in the GI tract Often form complexes in tissues called sulfur granules
392
Actinomycosis causing species
``` A. Israelli A. Naeslundii A. Viscosus A. Odontolyticus A. Meyeri ```
393
Most common cause of actinmycosis
A. Israelli
394
Actinomycosis
Relatively rare Chronic inflammatory condition Originates in tissues near mucosal surface Disease progresses slowly Characterized by a local hardening of tissue
395
Immune response to actinomyces
Very poor immune response -Ab can be detected Infections are typically chronic and only resolve with antibiotics
396
Most common site of actinomycosis
cervicofacial actinmycosis Due to poor dental hygiene Tooth extraction Trauma to mouth
397
Thoracic and abdominal actinomycosis
Rare Due to aspiration or trauma Diagnosis can be delayed due to vague symptoms Often mistaken for a malignancy Intrauterine contraceptive devices can lead to chronic endometriosis
398
Actinmycosis diagnosis
Patient history Presence of organims in pus Sulfur granules *** Anaerobic culture for at least 10 days
399
Actinmycosis Treatment
Penicillin G | High does
400
Nocardia natural reservoir
Soil
401
Nocardia type of pathogen
Aerobic gram positive filamentous bacilli Poorly staining
402
Nocardia are ______ aerobes
Strict
403
Nocardiosis can be found where of healthy individuals
Gingiva Respiratory tract NOT a commensal organism
404
2 forms of nocardiosis
Cutaneous Pulmonary (can become systemic) Disease is NOT spread person to person
405
Pathogenesis of nocardiosis
Unknown Can survive in phagocytes
406
Causes of nocardiosis
N. Asteroides | N. Farcinica
407
Pulmonary nocardiosis
Acute neutrophilic inflammation Pus formation and destruction of parenchyma Multiple abscesses may form
408
Cutaneous nocardiosis
Direct inoculation of N. Brasiliensis Infection can range from superficial pustule to more similar to actinomycosis (draining sinuses sulfur granules)
409
Immunity to Nocardia
Cell mediated immune response Th1 No humoral response
410
Nocardia diagnosis
Morphology Gram stain Acid fastness Culture requires 3-5 days
411
Nocardia treatment
Systemic sulfonamides alone or combined with trimethoprim
412
Anaerobes
Failure to grow in the presence of 10% oxygen Generate energy solely by fermentation
413
Oxygen tolerance
The ability for an organism to survive the presence of O2 for brief periods ot time
414
We are heavily colonized by anaerobic bacteria
Sebaceous glands Gingival crevices Lymphoid tissue in throat Intestinal and urogenital lumens
415
Anaerobic infections
Heavily colonized in us Most infections originate from our commensal microbiota Many anaerobes are also present in the environment
416
Clostridia
Gram + Bacilli Large spore forming
417
Clostridium exotoxins
Some can produce exotoxins Hemolysin Neutrotoxin Enterotoxin
418
Clostridium perfringens
Gram + Rod Hemolytic exotoxin Will produce large amounts of Hydrogen and CO2 in presence of carbs -Gas gangrene
419
Clostridium perfringens toxins : Alpha toxin
Phospholipase that hydroluzes lecithin and sphinogomyelin Leads to destruction of host cell membranes
420
Clostridium perfringens toxins : 0 Toxin
Pore forming Similar to streptomycin leads to altered capillary perameability Toxic to heart muscles
421
Clostridium perfringens toxins : enterotoxin
Forms pores in enterocyte membranes leading to changes in permeability alterations of tight junctions and eventual fluid loss
422
Gas gangrene
Clostridium myonecrosis Develops in traumatic wounds when contaminated with C. Perfringens or other histotoxic clostridia
423
C. Perfringens disease: food poisoning
Love growing in meat dishes especially at buffets Enterotoxin Ileum is most affect
424
C. Perfringens disease: food poisoning affects what area
Ileum is most affected by enterotoxin
425
C. Botulinum
Large Gram + Neurotoxin
426
Clostridium botulinum
Spores found in environment Prefer to grow in alkaline conditions Toxin is heat labile!
427
Foodborn botulims is considered
An intoxication not an infection
428
C. tetani
Slim Gram + Rod Found in the environment (spores)
429
Clostridium tetani type of pathogen
Strict anaerobic conditions
430
clostridium tetani neurotoxin
Produces potent neurotoxin
431
Tetanospasmin
Irreversible neurotoxin Lock jaw-spastic paralysis Prevent release of glycine and GABA
432
GABA
Is an inhibitory NT
433
Tetanospamsin is
Heat labile Antigenic Rapidly destroyed Readily neutralized
434
Tetanus route of passage
Usually enter though a deep penetrating wound Does not invade tissue
435
Tetanus incubation
4 days Masseter first
436
Tetanus treatment
Neutralize free toxin HTIG Benzodiazepines Vaccine preventative
437
C. Difficult
Gram + Can be found in environment and commensal
438
C. Efficient spore germination triggered by
Taurocholate Bile salt
439
C. Difficult produces 2 toxins
Toxin A Toxin B Disrupt cytoskeleton signal transduction
440
C. Difficult diarrhea
Mild Watery Bloody Can last weeks If Pseudomembranous colitis develops then it can become very severe
441
C. Difficile: Diagnosis
Stool culture
442
C. Difficile : treatment
Probiotics neutralize toxins Vancomycin
443
Peptostreptoccus
Gram + Anaerobic Opportunistic pathogens
444
Most common G+ anaerobic concussion in human oral cavity
P. Anaerobic | P micros
445
Peptostreptoccus usually involved in
Polymicrobial infections Abscesses Soft tissue infection Gingivitis periodontics
446
Bactericides fragilis
Gram - Capsulated Anaerobic commensal
447
Bactericides fragilis produce
Superoxide dismutates LPS is less toxic than most Gram -
448
Bactericides fragilis : polysaccharide capsule
Resistant to phagocytosis Hinders macrophage migration Helps with bacterial adhesion contributes to abscess formation
449
Bactericides fragilis : Enterotoxin
Some strain can produce Associated with watery self limiting diarrhea
450
Bactericides fragilis is a _____organism
Non invasive
451
Bactericides fragilis : effective antimicrobials
Clindamycin | Metronidazole
452
Lance field Groups
Serological classification based on major cell wall carbohydrates Groups A-H Many strep are un typeable No anti sera reacts to their cell wall antigens
453
Lance field Group A
Strep. Pyogenes
454
Lance field group B
Strep. Agalactiae
455
Pyogenic strep
Pus
456
Streptococci
Gram + Cocci arranged in chains Non spore forming Non motile Catalase negative
457
Streptococci capsule is variable
Carbohydrates Or Hyaluronic acid
458
Hemolysis Pattern
Alpha Beta Gamma
459
Hemolysis pattern of streptococcus: Alpha
Partial hemolysis and green discoloration of hemoglobin
460
Hemolysis pattern of streptococcus: Beta
Clear zone of complete hemolysis
461
Hemolysis pattern of streptococcus: Gamma
No zone of clearing
462
Disease caused by S. Pyogenes (group A strep): | GAS infections
Primarily infect respiratory tract bloodstream and skin 1 Suppurative diseases-direct damage by the organims 2Toxin mediated Disease-systemic response casued by exotoxins secreted in bloodstream 3 No suppurative sequelea-late manifestations autoimmune aberrant immunological reactions to GAS antigens
463
GAS is spread by
Respiratory droplets and direct person to person contact
464
S. Pyogenes virulence factors: M protein
Adhesins binds to keratinocytes
465
S. Pyogenes virulence factors: protein F
Fibronectin binding protein
466
S. Pyogenes virulence factors: Hyluronic acid
Anti phagocytic
467
S. Pyogenes virulence factors: hyaluronidase
Allows s. Pyogenes to spread through tissues
468
S. Pyogenes virulence factors: C5a peptidase
Degrades complement protein C5a blocking phagocyte chemotaxis
469
S. Pyogenes virulence factors: streptolysin S and O
Hemolysins that Lyme various host cells
470
S. Pyogenes virulence factors: streptokinase
Binds human plasminogen converting it to plasmid breaks fibrin clots allowing tissue spread
471
S. Pyogenes virulence factors: pyogenic exotoxins -superantigens
Fever neutropenia rash. Of scarlet fever
472
Pathogenesis of GAS infection: Adherence to mucosal surface
Pili M protein LTA Protein F
473
Pathogenesis of GAS: Adherence to sub corneal keratinocytes
M protein | Protein F
474
S. Pyogenes M protein
Resembles myosin functions: Binds to keratinocytes Prevents opsonization by complement
475
M protein type determines
Disease GAS can cause
476
Hyaluronic acid capsule
Purpose: Antiphagocytic structure Camouflage against the immune system Non antigenic -HA is found in human connective Tissue However capsule interferes with adherence to epithelial cellls
477
Secreted hyalruonidase
Digests the capsule allowing s. Pyogenes to spread through tissue
478
Streptolysin S and O
Pore forming toxin can lose red blood cells Also kills phagocytes Can lyse various host cells to real ease nutrients for growth
479
Streptolysin S
O2 stable
480
Streptolysin O
O2 labile
481
Streptokinase
Binds to plasminogen-enzymatic conversion to plasmin | -plasmin coated GAS can degrade and spread through fibrin resulting in invasive disease
482
Pyrogenic exotoxins
Secreted into bloodstream SpeA SpeB SpeC Cause rash associated with scarlet fever
483
SpeB
Most abundant Extracellular protein Cysteine protease-can degrade immunoglobulins and cytokines-prevents complement activation Degrades C3b
484
SpeA and SpeC
Bacterial superantigens No specifically active large subset of T cells Causing streptococcal toxic shock syndrome: StrepSAgs
485
___ immune response plays an imporatnt role in host defense against GAS infections
Innate
486
Most common manifestions of GAS
Acute Pharyngitis-strep throat Pyoderma-GAS infection for skin
487
GAS treatment
10 days penicillin
488
Skin infections caused by GAS
Impetigo Erysipelas
489
Gas-Clinical manifestations: Suppurative
Acute pharyngitis | Scarlet fever
490
Gas-Clinical manifestations: Non-Suppurative
Acute rheumatic fever Acute post streptococcal glomeruhulnphritis
491
Acute rheumatic fever
Hypersensitivity reaction caused by cross reacting antibodies effecting heart joints skin and brain
492
Acute rheumatic fever can be completely prevented by
Treating strep throat with a full course of penicillin
493
Symptoms of ARF
``` Fever Painful joints Chorea Heart murmur Non itchy rash ```
494
Acute Post streptococcal Glomerulonephritis
Following strep or impetigo Sympsmts Edema Tea colored urine Hypertension
495
Streptococcus penumoniae
Mitis group of Strem Gram + Alpha hemolytic Capsule antigenic carbohydrates
496
Pneumococcal spread
Person to person Direct contact Microaerosoles
497
Pneumococci virulence factors
Capsule Choline binding protein Pneumolysin Neuraminidase
498
Pneumococci virulence factors: Choline binding proteins
Adherence to host tissues
499
Pneumococci virulence factors: Pneumolysin
Transmembrane pore forming toxins
500
Pneumococci virulence factors: Neuraminidase
Cleaves sialic acid present in host mucin glycolipids and glycoproteins exposing binding sites
501
Pneumococci Capsule
90 serotypes Interferes with deposition of complement protein C3b on bacterial cell surface Antibodies specific to capsular proteins leads to classical complement pathway opsonophagocytosis
502
Pneumolysin
Pore forming toxins Released when cells lyse—not secreted Stimulates cytokines release Disrupts cilia of human respiratory epithelial cells-disruption of endothelial barrier-access to alveoli and blood stream
503
Pneumococcal disease is the leading cause of
``` Pneumonia Ottis media Acute purple to meningitis Bacteremia Other invasive infections ```
504
PPV23
Pneumococcal polysaccharide vaccine from 23 serotypes of s pneumoniae
505
PVC13
Pneumococcal conjugate vaccine Polysaccharide from 13 strains conjugated with protein
506
GBS-strep. Agalactiae
Leading cause of neonatal sepsis and meningitis in newborns Inhabits lower GI and female genital tracts
507
GBS: polysaccharide sialic acid capsule
Prevents opsonization and phagocytosis Type specific antibodies against GBS are protective against disease. Only 9 serotypes
508
S. Dysgalactiae
Pyogenes like | Causes bovine mastitis
509
S. Equi
Strangles in horses
510
Group D Streptococci
Enterococcus and non-enterococcus Normal flora of GI and genitourinary tracts
511
Enterococcus
Cause mostly nosocomial opportunistic infections BUT Vancomycin resistance enterococcus
512
Vivid as Streptococci
Alpha hemolytic strep Most common cause of subacute bacteria endocarditis -affects abnormal heart valves
513
Subacute Bacterial Endocarditis
bacterial infection on endocardium Usually develops when abnormal valves or heart disease is present ``` Symptoms: Fever Chills Muscle aches Abdominal pain Heart murmur ```
514
Staphylococcus
Cells are large and more round the strep Beta hemolytic Nonmotile Nonspore Catalase positive
515
Staph. Aureus: cell wall
Typical cell wall Containing peptidogluycan with lots of teichoic acid surrounded by polysaccharide capsule and surface proteins
516
Staph. Aureus: Polysaccharide capsule
Present in most strains but significance in human infections is unknown
517
Staph. Aureus: surface pro tines
Clumping Factors FnBP Surface protein A
518
Clumping Factors
Bind fibrinogen
519
FnBP
Binds fibronectin
520
Surface protein A
Binds the FC portion of IgG molecules Stimulate cytokines platelets and activates B cells
521
Staph. Aureus virulence factors
Toxins-cytolytic toxins cause cell lysis Alpha toxins PVL
522
Alpha toxins
Secreted by almost all S. Aureus Pore forming cytotoxin
523
PVL
Panton Valentine Leukocidin Active against platelets and neutrophils Causes tissue necrosis
524
Exfoliatin Toxin
Staph aureus virulence factor Protease that cleaves specific cell membrane fatty acids found not in keratizined epidermis of skin -Disrupts intraepidermal junctions —causes scalded skin syndrome
525
Staph Superantigens Toxins
SAgs secreted proteins that stimulate systemic effects when absorbed in the gut or when produced in vivo by multiplying bacteria
526
Enterotoxins of SAgs
Cause vomiting and diarrhea Very stable to boiling and digestive enzymes Can cause toxic shock syndrome
527
Toxic shock syndrome toxin
When released systemically-causes massive cytokines release. - strongly mite genie for T cells and are able to bind Class II MHC molecules on antigen presenting cells - activated up to 20% of all T cell non specifically
528
Staphylococcal Primary infections
Furuncle(boil) starts in follicle or gland Carbuncle(multiple boils) Impetigo Deep tissue lesion Pneumonia
529
Toxin mediate diseases (staph)
Can result from primary infections with strains that produce toxins Scaled skin Toxin shock syndrome Staph food poising
530
Staph aureus transmission
Nose picking Poor hygiene Fomite tranmission Survives drying can be spread from contaminated clothing
531
Staph aureus initial attachment by
FnBP
532
Staph. Aureus alpha toxin
Injures keratinocytes
533
Staph. Aureus immune evasion
Protein A antiphagocytic property PVL limits innate defens Coagulate and CIF-limit Host phagocytes Forms a boil
534
Staph. Aureus boil formation
Fibrin inflammatory cells and other components form a wall Spontaneously resolves- drainage of pus
535
Toxic shock syndrome
Results when toxin form a local infections entered bloodstream TSST 1 is most common from superantigens
536
Non menstrual TSS
Occur with strains that do not have TSST1
537
The only genus of gram negative cocci that frequently cause disease
Neisseria Usually diplococcic
538
Neisseria
Nonmotile Aerobic (but can grow anerobically) Obligate human pathogens
539
N. Gonococci
Localized inflammation Rarely lethal Can become serious if disseminated
540
Meningococci
Colonized the nasopharynx with no local sumpmts
541
Meningococci 3 general diseases
Uncomplicated bacteremia process Metastatic infecting of the meninges Overwhelming systemic infections-cicurlatory collapse and disseminated intravuasular coagulation
542
Meningococci _______ encapsulated and produces ______
Heavily Hemolysin
543
Gonococci upon introduction
Attach to columnar epitheal of cervix or ureatha
544
Gonococci adhesions controlled by
Phase variation Antigenic variation
545
Gonococci shed in genital secretions and do not
Have flagella and are not motile
546
Gonococci escape from phagocytosis
Extracellular s protease cleaves IgA1 removes Fc receptor allows for escape
547
Spread to ciliated and noncilaited cells gonococci
Attachment to nocilaited cells Ciliary stasis-cell motility slows then ceases Death of ciliated cells-slough from epithelial surface Exocytosis-vaculoules discharge bacteria into subepthieial connective tissues Do NOT secrete exotonsi
548
LPS and other cell wall components of gonococci
Cause cell damage Induce tumor necrosis factor=sloughing of ciliated cells Noncilaited cell lysis
549
Pelvic Inflammatory Disease
Gonococcal infection of female upper reproductive tract (Epididymitits ) ascent of organims into upper repro of men
550
Disseminated Gonococcal infections
DGI Can result from PID due to endotoxin Pustular lesions of skin
551
Primary reservoir for N. Meningitidis
Nasopharynx
552
N. Meningitidis attaches to
Nasopharyngeal epithelial cells and invades mucous membranes
553
______ pili attach N. Meningitidis to meninges
Type IV pili
554
N. Meningitidis invasion of blood only occurs
In individuals deficient in complement
555
Lipooligosaccharide
Damages host tissue | -elicits host inflammatory response, resulting in hemorrhaging of blood into skin and mucous membranes
556
Meningococci prevention
Vaccines Quadrivalent Tetravelnt
557
N. Gonorrhoeae Phase variation
Slipped strand mispairing | Encode outer membrane proteins
558
OPA
Colony opacited associated genes Encode outer membrane proteins
559
Opa’s presence
Results in neutrophil uptake Some gonococci lake opa and avoid phagocytosis
560
Haemophilus sp.
Small gram negative coccobacilli Encapsulated strains
561
Haemophilus sp. colonize
Upper respiratory tract
562
Haemophilus sp. attaches via
Type IV pili and outer membrane proteins
563
Haemophilus influenzae requires ___ and _____ for growth most only require
Hemin (xfactor) NAD+ NAD+
564
Lysed blood agar
Chocolate agar
565
Haemophilus influenzae access to hemin and NAD+ is through
Lysed blood
566
Non typeable H influenzae strains
Unencapsulatged
567
Typeable H. Influenzae strands
7 antigenically distinct capsular polysaccharides A-F +e’
568
Haemophilus influenzae type B
Most virulent Bacteremia Meningitis
569
Nontypeable strains of Haemophilus influenzae frequently cause
Respiratory tract disease in infant children and immunocompromised adults
570
H. Influenzae disease
Predominant bacterial pathogen of otitis media
571
H. Parainfluenzae
Sometimes causes pneumonia or bacterial endocarditis
572
H. Ducreyi
Causes chancroid. An std
573
H. Aphrophilus
Member of the normal flora of the mouth Occasionally causes bacterial endocarditis
574
H. Aegyptius
Causes conjunctivitis Brazilian purpuric fever
575
Haemophilus influenzae virulence factors
PRP Endotoxin IgA1 Pili and OM proteins
576
PRP-polyribosyl ribitol phospahte Capsuel
Resistance to phagocytosis Basis for Hib vaccine
577
IgA1 protease
Auto transport protein Directs their own secretion out of cell
578
Haemophilus biofilm formation
Pili are required
579
NTHI from biofilms
Within the human airways More resistant to host defenses Antibiotics are less effective
580
Hot defense against Haemophilus influenzae
Antibodies against capsule are protective Unencapsulated strains lack capsular polysaccharides and require development of novel surface targets
581
Treatment of Haemophilus influenzae
Resistant to penicillin (b lacatamase) Chloramphenicol drug of choice
582
Bordetella
Small gram negative coccobacilli Aerobic or microaerophilic
583
Bordetella colonized
Upper respiratory tract of adults Humans only known reservoir Causes whooping cough
584
Bordetella attaches to
Ciliated epithelial cells
585
Filamentous hemagglutinin
Binds to amino acids
586
Fimbriae and pertactin
Play important role in adherence to mucosal surfaces
587
Pertussis toxin
Paralyzes cilia | Induces inflammation
588
Bordetella do not invade
Epithelial cells But recently found in macrophage
589
Pertussis 3 stages
Cararrhal stage -Cold like (1-2 weeks) Paroxysmal stage -rapid coughs )1-6) Convalescent stage -gradual recovery (2-3 weeks)
590
Pertussis vaccination
Whole cell pertussis vaccine Acellular pertussis vaccine
591
Pseudomanoas aeruginosa
Gram negative bacillus Ubiquitos-found in soil Motile Aerobic
592
Pseudomonas aeruginosa motility by
One or several polar flagella Polar pili-twitching
593
Pseudomonas aeruginosa is _____
Aerobic Some strains grow aneraobically by nitrate respiration
594
Pseudomonas aeruginosa produce water soluble pigment that function as
Antibacterial
595
Pyocuanin
Blue green
596
Pyoverdin
Green
597
Fluorescein
Yellow fluorescence
598
Pseudomonas aeruginosa can be nonfermentative and use _____ just like ______
Indophenol oxidase just like nesseria
599
Pseudomonas aeruginosa need only ____ ___ and ____ sources
Acetate Ammonia as carbon Nitrogen
600
Pseudomonas aeruginosa: Persistence
``` Exotoxins A Phospholipase C Elastase Siderophores Mucous polysaccharide capsule ```
601
Pseudomonas aeruginosa: Dissemination
``` Toxin a Collagenase Elastase Exoenzymes Flagella Heat sable hemolysin Tissue damage by protease toxins ```
602
Phospholiapse C
Hydrolyzes phospholipids in eukaryotic membrane releasing useable phospahte
603
Siderophores
Compete with transferrin for iron Iron limitation causes increased production of elastase and exotoxin A -Damages tissues or creates conditions that make iron more accessible
604
Pseudomonas Encounter
Adheres to vegetables and plant matter In water taps drain -otitis externa-swimmers ear Hot tub -folliculitis, dermatitis
605
Pseudomonas opportunistic pathogen
Local or systemic breach of immune system immunocompromised patients
606
Pseudomonas do not adhere well to
Healthy epithelium Can enter through abrasions cuts etc Usually they don’t get far
607
Pseudomonas ability to spread and multiply depends on two things
Avoiding phagocytosis Successful adherence to a surface
608
Pseudomonas damage by Lipid A
Endotoxin Interacts with host TLR4 to initiate inflammatory response
609
Pseudomaonas damage
Adhesin Lipid A Core oligosacchardie Long O antigen side chains (responsible for reliant to human serum Ab and detergents
610
Pseudomonas Proteases
Multifunctional enzymes Elastase -cleaves elastin and collagen Cleaves proteinase inhibitors Cleaves immune system components LasA -serine protease that works with elastase to degrade elastin
611
Pseudomonas: Type III secretion system
Delivers virulence factors directly into host cells -transfer from bacterial cytoskeleton to host cytoplasm Come components are similar to flagella Target specific proteins on host cells Induced by host cell contact or low calcium levels
612
Pseudomonas aeruginosa and cystic fibrosis
do not adhere well to normal intact epithelium Cystic fibrosis respiratory cells binds more Pseudomonas aeruginosa than those of normal cells Thickened mucus inhibits normal ciliary clearance function
613
CFTR
Cystic firbrosis transmembrane conductance regulator
614
Dysfunction in Cystic fibrosis patients
Loss of Cl- transport | Hereditary
615
CFTR may cause
Decreased sialyation of surface glycolipids
616
Pseudomonas aeruginosa forms biofilms
Within the lungs Communities of bacterial cells that reside within a extracellular matrix Bacteria within biofilms are recalcitrant to antibiotic treatments and more resistant to host defenses
617
Sepsis
Severe systemic illness marked by hemodynamics derangement and organ malfunction brought about by the interaction of certain microbial products with hose reticulendetheal cells
618
Multi organ dysfunction syndrome
High cardiac output Lowered blood pressure Distributive shock
619
3 requirement of sepsis
Large population of infecting colonizing organims Presence of bacterial products that stimulate release of host cytokines Widespread dissemination of microbial products to hosts reticuloendothelial system
620
Lance field Groups
Serological classification based on major cell wall carbohydrates Groups A-H Many strep are un typeable No anti sera reacts to their cell wall antigens
621
Lance field Group A
Strep. Pyogenes
622
Lance field group B
Strep. Agalactiae
623
Pyogenic strep
Pus
624
Streptococci
Gram + Cocci arranged in chains Non spore forming Non motile Catalase negative
625
Streptococci capsule is variable
Carbohydrates Or Hyaluronic acid
626
Hemolysis Pattern
Alpha Beta Gamma
627
Hemolysis pattern of streptococcus: Alpha
Partial hemolysis and green discoloration of hemoglobin
628
Hemolysis pattern of streptococcus: Beta
Clear zone of complete hemolysis
629
Hemolysis pattern of streptococcus: Gamma
No zone of clearing
630
Disease caused by S. Pyogenes (group A strep): | GAS infections
Primarily infect respiratory tract bloodstream and skin 1 Suppurative diseases-direct damage by the organims 2Toxin mediated Disease-systemic response casued by exotoxins secreted in bloodstream 3 No suppurative sequelea-late manifestations autoimmune aberrant immunological reactions to GAS antigens
631
GAS is spread by
Respiratory droplets and direct person to person contact
632
S. Pyogenes virulence factors: M protein
Adhesins binds to keratinocytes
633
S. Pyogenes virulence factors: protein F
Fibronectin binding protein
634
S. Pyogenes virulence factors: Hyluronic acid
Anti phagocytic
635
S. Pyogenes virulence factors: hyaluronidase
Allows s. Pyogenes to spread through tissues
636
S. Pyogenes virulence factors: C5a peptidase
Degrades complement protein C5a blocking phagocyte chemotaxis
637
S. Pyogenes virulence factors: streptolysin S and O
Hemolysins that Lyme various host cells
638
S. Pyogenes virulence factors: streptokinase
Binds human plasminogen converting it to plasmid breaks fibrin clots allowing tissue spread
639
S. Pyogenes virulence factors: pyogenic exotoxins -superantigens
Fever neutropenia rash. Of scarlet fever
640
Pathogenesis of GAS infection: Adherence to mucosal surface
Pili M protein LTA Protein F
641
Pathogenesis of GAS: Adherence to sub corneal keratinocytes
M protein | Protein F
642
S. Pyogenes M protein
Resembles myosin functions: Binds to keratinocytes Prevents opsonization by complement
643
M protein type determines
Disease GAS can cause
644
Hyaluronic acid capsule
Purpose: Antiphagocytic structure Camouflage against the immune system Non antigenic -HA is found in human connective Tissue However capsule interferes with adherence to epithelial cellls
645
Secreted hyalruonidase
Digests the capsule allowing s. Pyogenes to spread through tissue
646
Streptolysin S and O
Pore forming toxin can lose red blood cells Also kills phagocytes Can lyse various host cells to real ease nutrients for growth
647
Streptolysin S
O2 stable
648
Streptolysin O
O2 labile
649
Streptokinase
Binds to plasminogen-enzymatic conversion to plasmin | -plasmin coated GAS can degrade and spread through fibrin resulting in invasive disease
650
Pyrogenic exotoxins
Secreted into bloodstream SpeA SpeB SpeC Cause rash associated with scarlet fever
651
SpeB
Most abundant Extracellular protein Cysteine protease-can degrade immunoglobulins and cytokines-prevents complement activation Degrades C3b
652
SpeA and SpeC
Bacterial superantigens No specifically active large subset of T cells Causing streptococcal toxic shock syndrome: StrepSAgs
653
___ immune response plays an imporatnt role in host defense against GAS infections
Innate
654
Most common manifestions of GAS
Acute Pharyngitis-strep throat Pyoderma-GAS infection for skin
655
GAS treatment
10 days penicillin
656
Skin infections caused by GAS
Impetigo Erysipelas
657
Gas-Clinical manifestations: Suppurative
Acute pharyngitis | Scarlet fever
658
Gas-Clinical manifestations: Non-Suppurative
Acute rheumatic fever Acute post streptococcal glomeruhulnphritis
659
Acute rheumatic fever
Hypersensitivity reaction caused by cross reacting antibodies effecting heart joints skin and brain
660
Acute rheumatic fever can be completely prevented by
Treating strep throat with a full course of penicillin
661
Symptoms of ARF
``` Fever Painful joints Chorea Heart murmur Non itchy rash ```
662
Acute Post streptococcal Glomerulonephritis
Following strep or impetigo Sympsmts Edema Tea colored urine Hypertension
663
Streptococcus penumoniae
Mitis group of Strem Gram + Alpha hemolytic Capsule antigenic carbohydrates
664
Pneumococcal spread
Person to person Direct contact Microaerosoles
665
Pneumococci virulence factors
Capsule Choline binding protein Pneumolysin Neuraminidase
666
Pneumococci virulence factors: Choline binding proteins
Adherence to host tissues
667
Pneumococci virulence factors: Pneumolysin
Transmembrane pore forming toxins
668
Pneumococci virulence factors: Neuraminidase
Cleaves sialic acid present in host mucin glycolipids and glycoproteins exposing binding sites
669
Pneumococci Capsule
90 serotypes Interferes with deposition of complement protein C3b on bacterial cell surface Antibodies specific to capsular proteins leads to classical complement pathway opsonophagocytosis
670
Pneumolysin
Pore forming toxins Released when cells lyse—not secreted Stimulates cytokines release Disrupts cilia of human respiratory epithelial cells-disruption of endothelial barrier-access to alveoli and blood stream
671
Pneumococcal disease is the leading cause of
``` Pneumonia Ottis media Acute purple to meningitis Bacteremia Other invasive infections ```
672
PPV23
Pneumococcal polysaccharide vaccine from 23 serotypes of s pneumoniae
673
PVC13
Pneumococcal conjugate vaccine Polysaccharide from 13 strains conjugated with protein
674
GBS-strep. Agalactiae
Leading cause of neonatal sepsis and meningitis in newborns Inhabits lower GI and female genital tracts
675
GBS: polysaccharide sialic acid capsule
Prevents opsonization and phagocytosis Type specific antibodies against GBS are protective against disease. Only 9 serotypes
676
S. Dysgalactiae
Pyogenes like | Causes bovine mastitis
677
S. Equi
Strangles in horses
678
Group D Streptococci
Enterococcus and non-enterococcus Normal flora of GI and genitourinary tracts
679
Enterococcus
Cause mostly nosocomial opportunistic infections BUT Vancomycin resistance enterococcus
680
Vivid as Streptococci
Alpha hemolytic strep Most common cause of subacute bacteria endocarditis -affects abnormal heart valves
681
Staphylococcus
Cells are large and more round the strep Beta hemolytic Nonmotile Nonspore Catalase positive
682
Staph. Aureus: Polysaccharide capsule
Present in most strains but significance in human infections is unknown
683
Staph. Aureus: surface pro tines
Clumping Factors FnBP Surface protein A
684
Clumping Factors
Bind fibrinogen
685
FnBP
Binds fibronectin
686
Surface protein A
Binds the FC portion of IgG molecules Stimulate cytokines platelets and activates B cells
687
Staph. Aureus virulence factors
Toxins-cytolytic toxins cause cell lysis Alpha toxins PVL
688
Alpha toxins
Secreted by almost all S. Aureus Pore forming cytotoxin
689
Staph Superantigens Toxins
SAgs secreted proteins that stimulate systemic effects when absorbed in the gut or when produced in vivo by multiplying bacteria
690
Enterotoxins of SAgs
Cause vomiting and diarrhea Very stable to boiling and digestive enzymes Can cause toxic shock syndrome
691
Toxic shock syndrome toxin
When released systemically-causes massive cytokines release. - strongly mite genie for T cells and are able to bind Class II MHC molecules on antigen presenting cells - activated up to 20% of all T cell non specifically
692
Staphylococcal Primary infections
Furuncle(boil) starts in follicle or gland Carbuncle(multiple boils) Impetigo Deep tissue lesion Pneumonia
693
Toxin mediate diseases (staph)
Can result from primary infections with strains that produce toxins Scaled skin Toxin shock syndrome Staph food poising
694
Staph aureus transmission
Nose picking Poor hygiene Fomite tranmission Survives drying can be spread from contaminated clothing
695
Staph aureus initial attachment by
FnBP
696
Staph. Aureus alpha toxin
Injures keratinocytes
697
Staph. Aureus immune evasion
Protein A antiphagocytic property PVL limits innate defens Coagulate and CIF-limit Host phagocytes Forms a boil
698
Staph. Aureus boil formation
Fibrin inflammatory cells and other components form a wall Spontaneously resolves- drainage of pus
699
Toxic shock syndrome
Results when toxin form a local infections entered bloodstream TSST 1 is most common from superantigens
700
Non menstrual TSS
Occur with strains that do not have TSST1
701
The only genus of gram negative cocci that frequently cause disease
Neisseria Usually diplococcic
702
Neisseria
Nonmotile Aerobic (but can grow anerobically) Obligate human pathogens
703
N. Gonococci
Localized inflammation Rarely lethal Can become serious if disseminated
704
Meningococci
Colonized the nasopharynx with no local sumpmts
705
Meningococci 3 general diseases
Uncomplicated bacteremia process Metastatic infecting of the meninges Overwhelming systemic infections-cicurlatory collapse and disseminated intravuasular coagulation
706
Meningococci _______ encapsulated and produces ______
Heavily Hemolysin
707
Gonococci upon introduction
Attach to columnar epitheal of cervix or ureatha
708
Gonococci adhesions controlled by
Phase variation Antigenic variation
709
Gonococci shed in genital secretions and do not
Have flagella and are not motile
710
Gonococci escape from phagocytosis
Extracellular s protease cleaves IgA1 removes Fc receptor allows for escape
711
Spread to ciliated and noncilaited cells gonococci
Attachment to nocilaited cells Ciliary stasis-cell motility slows then ceases Death of ciliated cells-slough from epithelial surface Exocytosis-vaculoules discharge bacteria into subepthieial connective tissues Do NOT secrete exotonsi
712
LPS and other cell wall components of gonococci
Cause cell damage Induce tumor necrosis factor=sloughing of ciliated cells Noncilaited cell lysis
713
Pelvic Inflammatory Disease
Gonococcal infection of female upper reproductive tract (Epididymitits ) ascent of organims into upper repro of men
714
Disseminated Gonococcal infections
DGI Can result from PID due to endotoxin Pustular lesions of skin
715
Primary reservoir for N. Meningitidis
Nasopharynx
716
N. Meningitidis attaches to
Nasopharyngeal epithelial cells and invades mucous membranes
717
______ pili attach N. Meningitidis to meninges
Type IV pili
718
N. Meningitidis invasion of blood only occurs
In individuals deficient in complement
719
Lipooligosaccharide
Damages host tissue | -elicits host inflammatory response, resulting in hemorrhaging of blood into skin and mucous membranes
720
Meningococci prevention
Vaccines Quadrivalent Tetravelnt
721
N. Gonorrhoeae Phase variation
Slipped strand mispairing | Encode outer membrane proteins
722
OPA
Colony opacited associated genes Encode outer membrane proteins
723
Opa’s presence
Results in neutrophil uptake Some gonococci lake opa and avoid phagocytosis
724
Haemophilus sp.
Small gram negative coccobacilli Encapsulated strains
725
Haemophilus sp. colonize
Upper respiratory tract
726
Haemophilus sp. attaches via
Type IV pili and outer membrane proteins
727
Haemophilus influenzae requires ___ and _____ for growth most only require
Hemin (xfactor) NAD+ NAD+
728
Lysed blood agar
Chocolate agar
729
Haemophilus influenzae access to hemin and NAD+ is through
Lysed blood
730
Non typeable H influenzae strains
Unencapsulatged
731
Typeable H. Influenzae strands
7 antigenically distinct capsular polysaccharides A-F +e’
732
Haemophilus influenzae type B
Most virulent Bacteremia Meningitis
733
Nontypeable strains of Haemophilus influenzae frequently cause
Respiratory tract disease in infant children and immunocompromised adults
734
H. Influenzae disease
Predominant bacterial pathogen of otitis media
735
H. Parainfluenzae
Sometimes causes pneumonia or bacterial endocarditis
736
H. Ducreyi
Causes chancroid. An std
737
H. Aphrophilus
Member of the normal flora of the mouth Occasionally causes bacterial endocarditis
738
H. Aegyptius
Causes conjunctivitis Brazilian purpuric fever
739
Haemophilus influenzae virulence factors
PRP Endotoxin IgA1 Pili and OM proteins
740
PRP-polyribosyl ribitol phospahte Capsuel
Resistance to phagocytosis Basis for Hib vaccine
741
IgA1 protease
Auto transport protein Directs their own secretion out of cell
742
Haemophilus biofilm formation
Pili are required
743
NTHI from biofilms
Within the human airways More resistant to host defenses Antibiotics are less effective
744
Hot defense against Haemophilus influenzae
Antibodies against capsule are protective Unencapsulated strains lack capsular polysaccharides and require development of novel surface targets
745
Treatment of Haemophilus influenzae
Resistant to penicillin (b lacatamase) Chloramphenicol drug of choice
746
Bordetella
Small gram negative coccobacilli Aerobic or microaerophilic
747
Bordetella colonized
Upper respiratory tract of adults Humans only known reservoir Causes whooping cough
748
Bordetella attaches to
Ciliated epithelial cells
749
Filamentous hemagglutinin
Binds to amino acids
750
Fimbriae and pertactin
Play important role in adherence to mucosal surfaces
751
Pertussis toxin
Paralyzes cilia | Induces inflammation
752
Bordetella do not invade
Epithelial cells But recently found in macrophage
753
Pertussis 3 stages
Cararrhal stage -Cold like (1-2 weeks) Paroxysmal stage -rapid coughs )1-6) Convalescent stage -gradual recovery (2-3 weeks)
754
Pertussis vaccination
Whole cell pertussis vaccine Acellular pertussis vaccine
755
Pseudomanoas aeruginosa
Gram negative bacillus Ubiquitos-found in soil Motile Aerobic
756
Pseudomonas aeruginosa motility by
One or several polar flagella Polar pili-twitching
757
Pseudomonas aeruginosa is _____
Aerobic Some strains grow aneraobically by nitrate respiration
758
Pseudomonas aeruginosa produce water soluble pigment that function as
Antibacterial
759
Pyocuanin
Blue green
760
Pyoverdin
Green
761
Fluorescein
Yellow fluorescence
762
Pseudomonas aeruginosa can be nonfermentative and use _____ just like ______
Indophenol oxidase just like nesseria
763
Pseudomonas aeruginosa need only ____ ___ and ____ sources
Acetate Ammonia as carbon Nitrogen
764
Pseudomonas aeruginosa: Persistence
``` Exotoxins A Phospholipase C Elastase Siderophores Mucous polysaccharide capsule ```
765
Pseudomonas aeruginosa: Dissemination
``` Toxin a Collagenase Elastase Exoenzymes Flagella Heat sable hemolysin Tissue damage by protease toxins ```
766
Phospholiapse C
Hydrolyzes phospholipids in eukaryotic membrane releasing useable phospahte
767
Siderophores
Compete with transferrin for iron Iron limitation causes increased production of elastase and exotoxin A -Damages tissues or creates conditions that make iron more accessible
768
Pseudomonas Encounter
Adheres to vegetables and plant matter In water taps drain -otitis externa-swimmers ear Hot tub -folliculitis, dermatitis
769
Pseudomonas opportunistic pathogen
Local or systemic breach of immune system immunocompromised patients
770
Pseudomonas do not adhere well to
Healthy epithelium Can enter through abrasions cuts etc Usually they don’t get far
771
Pseudomonas ability to spread and multiply depends on two things
Avoiding phagocytosis Successful adherence to a surface
772
Pseudomonas damage by Lipid A
Endotoxin Interacts with host TLR4 to initiate inflammatory response
773
Pseudomaonas damage
Adhesin Lipid A Core oligosacchardie Long O antigen side chains (responsible for reliant to human serum Ab and detergents
774
Pseudomonas Proteases
Multifunctional enzymes Elastase -cleaves elastin and collagen Cleaves proteinase inhibitors Cleaves immune system components LasA -serine protease that works with elastase to degrade elastin
775
Pseudomonas: Type III secretion system
Delivers virulence factors directly into host cells -transfer from bacterial cytoskeleton to host cytoplasm Come components are similar to flagella Target specific proteins on host cells Induced by host cell contact or low calcium levels
776
Pseudomonas aeruginosa and cystic fibrosis
do not adhere well to normal intact epithelium Cystic fibrosis respiratory cells binds more Pseudomonas aeruginosa than those of normal cells Thickened mucus inhibits normal ciliary clearance function
777
CFTR
Cystic firbrosis transmembrane conductance regulator
778
Dysfunction in Cystic fibrosis patients
Loss of Cl- transport | Hereditary
779
CFTR may cause
Decreased sialyation of surface glycolipids
780
Pseudomonas aeruginosa forms biofilms
Within the lungs Communities of bacterial cells that reside within a extracellular matrix Bacteria within biofilms are recalcitrant to antibiotic treatments and more resistant to host defenses
781
Sepsis
Severe systemic illness marked by hemodynamics derangement and organ malfunction brought about by the interaction of certain microbial products with hose reticulendetheal cells
782
Multi organ dysfunction syndrome
High cardiac output Lowered blood pressure Distributive shock
783
3 requirement of sepsis
Large population of infecting colonizing organims Presence of bacterial products that stimulate release of host cytokines Widespread dissemination of microbial products to hosts reticuloendothelial system

Micro/Immuno (3 decks)

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