8_Gram Positives iI Flashcards
1
Q
What are the 3 key diseases caused by S. pneumoniae?
A
-
acute bacterial pneumonia
- part of normal nasopharyngeal flora (5-40%)
- major causative agent of pneumonia in the aged and immunocompromised patients
- Sxs: fever, cough with sputum, dull chest
-
otitis media
- middle ear infection
-
meningitis
- most common cause of meningitis
- Sxs: fever, neck pain, headache
2
Q
What is the Lancefield grouping of S. penumoniae?
A
NONE! It’s a non-Lancefield pathogen
3
Q
What is the S. pneumoniae vaccine?
(structure and serotypes)
A
- Pneumovax
- Structure is a polysaccharide capsule w/ multiple serotypes
- Capsular serotypes: some strains are more virulence than others
- Original vaccine was targeted against the 6 most virulent serotypes
4
Q
multivalent vaccine:
define
A
- multivalence means it is directed against multiple serotypes;
- antigenic portion of the polysaccharide from each of the multiple serotypes is attached to a carrier so the vaccine can be directed against multiple serotypes
5
Q
of the serotypes in the Streptococcus pneumoniae vaccine, which serotype is most virulent?
A
serotype 4 is more virulent than serotype 19A
6
Q
Is S. pneumoniae competent?
What does this allow it to do?
A
- S. pneumoniae is naturally competent
- can take up DNA by transformation and –> incorporate the new DNA by RecA-mediated homologous recombination.
7
Q
how are more virulent strains of S. pneumoniae able to escape a vaccine?
A
- Natural competence allows more virulent strains (such as serotype 4) –> to pick up the capsule from less virulent strains (such as serotype 19A).
- This allows them to escape the vaccine.
8
Q
Why do we need 13- and 23-valent vaccines to combat the S. penumoniae bacteria?
A
- Because of natural competence and the ability of more virulent strains to pick up the capsule from less virulent strains
- Need the 13 and 23 valent vaccines to cover additional serotypes. (Pneumovax13 and Pneumovax23)
9
Q
S. pneumoniae:
distinguishing features
A
- Gram-positive, lancet-shaped diplococci
- Catalase negative
- Quellung rxn (capsular swelling) – positive
10
Q
GBS (Group B Streptococcus);
Streptotoccus agalactiae
location, frequency, transmission, sxs
A
- found in normal vaginal flora: 10-30% of women
- transmitted
- birth or by carrier or by contaminated materials
- newborns are sensitive due to underdeveloped normal flora
- Sxs may not develop until the infant goes home
- Therefore, pregnant women are screened and treated w/ Abx prior to birth
11
Q
Diseases caused by Group B Streptoccocus, and sxs
(Streptococcus agalactiae)
A
- Neonatal Meningitis
- sxs: fever, lethargy, poor feeding, seizures
- can be cultured from CSF after lumbar puncture
- Neonatal Pneumonia
•cyanosis, tachypnea (rapid respiration), respiratory distress
- Post-partum Endometritis
12
Q
Group B Streptococci (S. agalactiae):
distinguishing features
A
- Gram-positive cocci in short chains
- Found in CSF
- Systemic can be found in blood sample
- CAMP test positive
- CAMP factor enhances hemolysis caused by S. aureus hemolysins
13
Q
What is the CAMP Test Positive?
A
- identify group B βeta-hemolytic streptococci (Streptococcus agalactiae) based on their formation of a substance (CAMP factor) that enlarges the area of hemolysis formed by the β-hemolysin elaborated from Staphylococcus aureus.
14
Q
Which 2 genera are Group D Enterococci found in?
A
Group D Enterococci is a diverse group containing bacteria from 2 different genera:
- Enterococcus and
- Streptococcus
15
Q
Enterococci:
location, diseases it can cause, and 2 examples
A
- Location: GI tract normal flora; nosocomial pathogens (aka found in the hospital and are Abx-resistant)
- Can cause:
- septicemia
- UTI
- endocarditis
- Ex. E. faecium, and E. faecalis
16
Q
How are commensal bacteria converted to pathogens?
A
Virulence factors that are acquired from mobile genetic elements (plasmids, transposons, and PAIs- pathogenicity island) –> can convert the commensals to pathogens
17
Q
What can result from antibiotic resistance?
A
Can lead to:
- multi-drug resistant strains (MDR)
- vancomycin resistance enterococci (VRE)
18
Q
Enterococci (Group D):
distinguishing factors
A
- Enterococci
- Gram-positive cocci that often occur in singles, pairs (diplococci) or short chains
- Catalase negative
- PYR positive (Pyrrolidonyl Arylamidase (PYR) test)
- Grows in bile salts and 6.5% NaCl
19
Q
Corynebacterium diphtheriae:
distinguishing factors
(shape, location, transmission)
A
- Gram-positive club-shaped rod
- does not disseminate but forms pseudomembrane in the back of the throat, including:
- fibrin
- leukocytes
- necrotic epithelial cells
- bacteria
20
Q
Diphtheria toxin
(structure, function, and targets of the)
A
- Produced by C. Diphtheriae
- Structure
- AB toxin
- B subunit protective factor
- A subunit is ADP ribosylates Elongation Factor 2 (EF2) of the ribosome, inhibiting protein synthesis and killing the cell
- Targets
- heart cells –> arrhythmia, myocarditis
- nerve cells –> peripheral and cranial palsy
21
Q
Listeria monocytogenes:
distinguishing factors
(structure, location, diseases caused)
A
- Gram-positice rod
- Grows intracellularly;
- Tx by:
- food borne illness (milk, soft cheeses, butter, and deli meats)
- spreads into blood stream –> to CNS
- Can cause:
- meningitis in fetus if mother ingests it (even if mother is asymptomatic)
- can cause meningitis is immunosuppressed patientsa and sometimes pregnant women
22
Q
Define and describe the unique mechanism for:
spreading L. monocytogenes between eukaryotic cells
A
- “Host Cell Actin Polymerization”
- Process
- Internalin (surface protein found on L. monoctogenes) allows invasion
- Listeria lysin O (LLO) allows escape into the cytoplasm,
- then the bacteria polymerize host actin to move between eukaryotic cells
23
Q
Spirochetes:
distinguishing characteristics
A
- Gram-negative bacteria
- too thin to see by light microscopy
- uses dark-field microscopy is commonly used.
24
Q
Endoflagella:
define
A
- structure
- special flagella of the spirochetes;
- wound around their tiny cork-screw shape;
- these endoflagella together form what is called an axial filament
- location
- sits between outer membrane and peptidoglycan layer
25
what are the 3 genera that are pathogenic for man?
* **Treponema** (Syphilis)
* **Borrelia** (Relapsing fever and Lyme disease)
* **Leptospira** (Leptospirosis)
26
1. Which bacteria causes **Syphilis**?
2. How is it transmitted?
3. Does the outer membrane have LPS?
1. Treponema pallidum
2. Usually sexually transmitted; causes a chronic illness
3. The Treponema pallidum does NOT HAVE LPS in its outer membrane
27
sequential stages of:
Syphilus
1. Inoculation by sexual contact
2. **Primary** syphilis
* **chancre,** which is a sore on the surface of the tongue - infectious
3. **Secondary** syphilis
* rash and mucocutaneous lesions - infectious
4. **Latent** syphilis
* no symptoms; relapses to secondary syphilis
5. **Tertiary** syphilis
* invasion into cardiac or nerve cells (brain)
28
Describe the step:
**Primary Syphilis**
* **long incubation --\>**
* to a lesion that starts as a painless papule and forms an ulcer (**chancre**)
* **contagious** throughout entire period
29
Describe the step:
Secondary syphilis
* mucocutaneous lesions and rash
* very contagious
* 2-8 wks after primary chancre
* (the primary and secondary stages may overlap)
30
Describe the step:
## Footnote
**Latent Syphilus**
* asymptomatic
* can cycle back to secondary syphilis (relapse) until there are enough antibodies to prevent more relapses
* relapses becomes less severe with time
31
Describe the step:
## Footnote
**Tertiary syphilis**
* Affects the nervous and cardiovascular disease, most commonly
* Due to growth of spirochetes in the brain or heart disease
* occurs in untreated patients
32
CC: Congenital Syphilis
| (effects, and sxs)
* Treponema pallidum passes the placenta to the fetus causing death or skeletal system defects
* Newborns will have mucosal patches which are infectious
33
What are the laboratory tests for Treponema pallidum?
* Diagnosed by **darkfield microscopy**, or
* **fluorescent microscopy or by serology** (especially in secondary syphilis)
34
Tx and prevention of syphilis
* Treatment: penicillin (usually)
* alternatives are tetracycline, doxycycline, and azithromycin
* Prevention:
* safe sex practices; all whoa re infected and their sexual contacts should be treated
35
Borrelia burgdorferi:
shape, seen with
* large spirochete; (lrgst in size of pathogenic spirochetes)
* can be seen w/ light microscope
* stained w/ Gram stain, Giemsa, or Wright stain
36
Which bacteria causes **Lyme disease**?
How is it transmitted? Sxs
* *Borrelia burdorferi* causes Lyme disease
* transmitted by the Deer tick (most common tick-transmitted disease)
* variety of sxs, affecting multiple body systems
37
describe the lifecycle of the Ixodes tick
* Deer tick (Ixodes scapularis) takes 2 years to mature
* 1st year - nymphs feeding on small mammals
* 2nd year - adults and feed on deer.
* In both cases the tick becomes **infected with Borrelia burgdorferi when it feeds on small mammals** (esp. white footed mice).
* **Infected nymphs or adults can infect a person but it is usually a nymph (primary route).**
38
First stage, Second stage, and Late stage of
Lyme disease
* First stage:
* **nymphs** are small ticks; people don't usually remember being bitten
* develops **bulls-eye rash** (erythema migrans) at bite site
* sxs: fever, headache, myalgia, joint pain
* Second stage:
* days - months later; patient develops neurologic or cardiac abnormalities
* Late stage:
* arthritis in 2/3 untreated patients
39
Diagnosis and tratment for:
Lyme's disease
Diagnosis
* usually based on hx and clinical observations
* Abx titers to B. bergdorferi can be confirmed by immunofluorescent assay or ELISA
* positive results can be confirmed by Western blot
Treatment
* Abx should be initiated as soon as possible
* Doxycycline and amoxicillin for tx
Prevention
* prevention is focused on preventing tick bites (clothing, insect repellents)
* check for ticks and remove immediately
