Micro, Ass 4, Renee’s Questions

1.     What are the 3 main species of Staphylocci that cause infections in humans?
1.     S. aureus, S. epidermidis, S. saprophyticus
2.     What makes Staphylcocci so hardy?
2.     grow in many different media, resistant to drying out.
3.     What are the results of a catalase test with Staph?
3.     Positive
4.     Which Staph species is the only one that is coagulase positive?
4.     S. aureus
5.     What makes a coagulase test positive?
5.     Coagulase is an enzyme bound to S. aureus that activates prothrombin, converting fibrinogen to fibrin, clotting the colonies and fibrin.
6.     How is coagulase anti-phagocytic?
6.     Fibrinogen bound to bacteria masks them from phagocytes.
7.     When you think of Pus-Filled Abscesses what pyogenic cocci should you think of?
7.     S. aureus
8.     What is S. aureus’ favorite niche?
8.     anterior nares
9.     What hemolysis class are S. aureus?
9.     ?-hemolytic
10.  A gram stain showing clusters of Gram+ organisms would be what organism?
10.  Staphylococci
11.  Gram+, Catalase +, Coagulase Negative organism could be what?
11.  S. epidermidis or S. saprophyticus
12.  What species of staph colonizes the GI tract and perineum?
12.  S. saprophyticus
13.  What species of staph produces a polysaccharide capsule?
13.  S. aureus
14.  What species of staph produces a very heavy capsule called slime?
14.  S. epidermidis
15.  What type of test is very rapid with >95% sensitivity?
15.  Fluorescent 16S rRNA
16.  Why do biofilms cause such a problem in treatment?
16.  Bacteria within biofilms are essentially dormant and tolerant to antibiotic-induced killing
17.  Which species of Staph do biofilms cause the biggest problem? Why?
17.  S. epi; can cause IV infections and infections of prosthetic devices
18.  How do capsules increase virulence?
18.  have anti-phagocytic effects
19.  What is the acronym for the surface adhesins?
19.  MSCRAMM (microbial surface component reacting with adherence matrix molecules)
20.  How do MSCRAMMs bind to cell walls?
20.  covalently bound by membrane bound enzyme called sortase
21.  How does the enzyme, sortase, bind MSCRAMMs?
21.  cleaves an LPXTG motif at the C-terminus of the proteins (between T and G); attaches to un-crosslinked peptide cros bridge of the peptidoglycan layer.
22.  What are some MSCRAMMs?
22.  protein A, clumping factors A and B (clfA, clfB), collagen-binding protein (can), fibronectin-binding protein B (fnbB)
23.  What disease is caused by exfoliatin?
23.  Scalded skin syndrome
24.  What is exfoliatin?
24.  epidermolytic exotoxin
25.  How does exfoliatin cause blistering of the skin?
25.  toxins are dispersed and become localized in stratum granulosum, degrades desmoglein-1
26.  How do Superantigens work?
26.  binds to both MHC-class II and the T cell receptor and activates up to 20% of the entire lymphocyte population
27.  What do superantigens cause?
27.  massive secretion of cytokines, driving an overwhelming inflammatory response, endotoxin-like shock.
28.  How many different superantigens can S. aureus express?
28.  15
29.  What are the symptoms of Toxic Shock Syndrome?
29.  high fever, diffuse erythematous rash followed by desquamation
30.  How is TSST-1 different than other SAgs?
30.  can cross the mucosal barrier and distribute throughout the body.
31.  What is the main causes of food poisoning?
31.  Enterotoxins
32.  What is the difference between intoxication and infection?
32.  Live bacteria don’t have to be present to cause an intoxication
33.  T/F Toxins can be eliminated by cooking.
33.  F – Toxins are heat stable and not denatured by cooking
34.  How soon after ingestion does a food intoxication cause disease? How long does it usually last?
34.  2-6 hours; 6-12 hours
35.  Is there Fever associated with food poisoning?
35.  NO
36.  What does MRSA contain that makes it so resistant to antibiotics?
36.  Resistance island – staphylococcal chromosome cassette mec; mec encodes an unusual penicillin-binding protein
37.  How do ?-lactams kill bacteria?
37.  Analogs of D-ala-D-ala terminus of the peptide crossbridges, inhibit cell wall formation by binding to the penicillin-binding proteins.
38.  How does S. aureus resist penicillin?
38.  secrets penicillinase to hydrolyze penicillin
39.  What is the mechanism of methicillin resistance?
39.  mecA gene encodes PBP2A with low affinity for all ?-lactams.
40.  Where can staph cause disease?
40.  Anywhere the blood goes.
41.  What clinical syndrome caused mostly by S. aureus involves only epidermis with Red macula that evolve into blisters due to epidermolytic toxins?
41.  Impetigo
42.  What is Folliculitis?
42.  Pyoderma that involves the hair follicle and immediate surroundings
43.  If a patient has recurrent furuncles, what should they be tested for and why?
43.  nasal carriage of CA-MRSA; CA-MRSA is a frequent cause of furuncles that can progress to abscesses and cellulitis
44.  What type of infection presents with fever, tachycardia, hypotension, dyspnea, and a new cardiac murmur?
44.  Infective Endocarditis
45.  What are the main risk factors for Infective Endocarditis?
45.  IV drug use, being elderly with valve sclerosis, being a patient with intravascular prostheses, being on hemodialysis
46.  Which type of Endocarditis is easier to treat?
46.  Right-side endocarditis
47.  What is the percentage of hospital acquired pneumonia that is caused by S. aureus?
47.  20-30%
48.  What is the leading cause of Osteomyelitis?
48.  S. aureus
49.  When you think of indwelling medical devices, biofilms, indolent infections, and drug resistance what comes to mind?
49.  CoagNS!!!
50.; What is the most common cause of primary bacteremia? Why?
50.; S. epi; because its niche is the skin and we shove stuff through it all the time.
51.  Compare the pathogenicity of S. aureus and S. epi.
51.  S. aureus; true human pathogen with enough virulence factors to cause infection in a health person
52.  What type of adhesion does S. epi express?
52.  fibrinogen, fibronectin, collagen, vitronectin and elastin.
53.  T/F Polysaccharide intercellular adhesion is a major part of S. epi and S. aureus biofilms.
53.  F – major part of S. epi, not S. aureus
54.  What allows biofilms to detach and spread to other potential sites?
54.  Dispersal products – phenol-soluble modulins (PSMs)
55.; What is PGA?

55.; Poly-gamma-DL-glutamic acid; antiphagocytic capsular material.

;

It is found in the capsules of S. epi species which allows them to colonize skin and mucosal surfaces.

56.  What organisms make PGA?
56.  S. epi (facilitates colonization of and persistence on skin, makes sense why S. epi has it and S. a does not)
57.  What types of bacteriocins does S. epi make?
57.  epidermin, Pep5 and epilancin
58.  Infections in Cardiac Devices is mostly cause by which organisms?
58.  CoagNS, 50-60% or cases
59.; Orthopedic prosthetic device infections can be classified as early, delayed, and late. Which type of organisms are associated with each classification?
59. Early: within 3 months ; S. aureus Delayed: 3 months ; 2 years ;CoagNS Late: longer than 2 years ; hematogenous inoculation of organisms form another source
60.  A patient with a recent CF shunt placement and local signs of inflammation, nausea and vomiting most likely has an infection from what type of organism?
60.  CoagNS – S. Epi
61.  Why is it hard to determine if S. epi is the culprit of an infection?
61.  inhabit human skin and mucous and are considered part of the normal microbiota in humans; very likely to show up in any sample.
62.  How do Streptococci grow?
62.  in chains
63.  What is the result of a catalase test on a streptococcal species?
63.  Negative
64.  How are streptococci distinguished from Neisseria?
64.  Streptococci are Oxidase negative and Nisseria species are oxidase positive.
65.  What Lancefield group is S. pyogenes?
65.  Group A
66.  What is the most common bacterial cause of acute pharyngitis?
66.  S. pyogenes
67.  T/F S. pyogenes is pyogenic
67.  T – Duh that’s practically it’s name
68.  What type of hemolytic reaction does S. pyogenes have?
68.  ?
69.  What does it mean to be nutritionally fastidious?
69.  require specialized environments due to complex nutritional requirements
70.  Why do the S. pyogenes colonies have a mucoid appearance?
70.  produce copious amounts of a hyaluronic acid capsule
71.  Why is the S. pyo capsule a poor immunogen?
71.  because it is structurally identical to human HA
72.  What is the major somatic virulence factor of S. pyogenes?
72.  M protein
73.  What makes strains of S. pyogenes that are rich in M protein resistant to phagocytosis?
73.  inhibition of the alternate pathway for activating complement
74.  How do M-related proteins cooperate in the antiphagocytosis effect?
74.  Bind IgG or IgA at the non-antigen-binding site.
75.  What is a hemolysin?
75.  exotoxin produced by bacteria that cause lysis of red blood cells
76.; What type of hemolysins does S. pyogenes produce?
76.; Streptolysin O (SLO) and SLS
77.  Which hemolysin is labile in the presence of oxygen?
77.  Streptolysin O
78.  How is SLO inhibited?
78.  reversibly inhibited by oxygen
79.; What can be measured to indicate a recent Group A streptococcal infection?
79.; anti-SLO antibodies
80.  Which Lancefield group is responsible for the majority of the bacterial pharyngitis?
80.  Group A
81.  What is the drug of choice for S. pyogenes?
81.  penicillin
82.  What type of skin infection is a superficial purulent pyoderma with weeping vesicles that form honey-colored crusts?
82.  Impetigo
83.  What organisms primarily cause pyoderma impetigo?
83.  ?-hemolytic streptococci and S. aureus
84.  What is a type of streptococcal cellulitis?
84.  Erysipelas
85.  What is the treatment for Necrotizing fasciitis?
85.  Debridement of tissue, broad spectrum antibiotics immediately, massive amounts of IV fluids, monitor cardiac out put closely
86.  What are 2 forms of Nonsuppurative Poststreptococcal Sequelae?
86.  Acute Rheumatic Fever and Acute Glomerulonephritis
87.  What are the guidelines for Diagnosis of Initial Attack of ARF, The Jones Criteria?
87.  Major Manifestations: Carditis
Polyarthritis
Chorea
Erythema marginatum (rash on trunk and limbs, charactaristic of ARF)
88.  What are the Guidelines for Diagnosis of AGN?
88.  Major Manifestations: Edema
Hypertension
Hematuria
Proteinuria
Malaise, headache, backache
89.  What is the Treatment for AGN?
89.  Benzathine penicillin
90.  What is Group B Strep resistant to?
90.  Bacitracin
91.  What is the major virulence factor for GBS?
91.  Capsule, Capsule, Capsule!
92.  What binds with factor H to downregulate complement deposition?
92.  Surface ?-protein (GBS?)
93.  Why is GBS testing in pregnancy so important?
93.  GBS very harmful to neonate – septicemia, respiratory distress, meningitis
94.; Which organism is present in dental plaque?

94.; Viridans Streptococci

Typically S. mutans

95.  What is the hemolysis of Viridans Streptococci?
95.  ?-hemolytic
96.  What is an important cause of nosocomial infections?
96.  Enterococcus
97.  How do you distinguish between Viridans Streptococci and pneumococci?
97.  Viridans resistant to optochin, pneumococci susceptible to optochin
98.  How is pneumococci diagnosed?
98.  culture sputum, blood or CSF
99.  What are the risk factors for Pneumonia?
99. viral infection
chronic pulmonary disease
splenic disorders
alcoholism
100.;;;;;;; What are preventative measures against pneumococcal infections?
100. Pneumovax Prevnar13 Flu Vaccine!
101.        What are the symptoms of Bacterial meningitis?
101.       Headache, fever, vomiting, photophobia, stiff neck, irritability, and varying degrees of neurologic dysfunction
102.        What CSF findings are associated with meningitis?
102.       Large #PMNs, reduced glucose, elevated protein
103.        What is the most common cause of bacterial meningitis in the US?
103.       Pneumococcus
104.        What combination of drugs are often used in the treatment of bacterial meningitis?
104.       cephalosporin and vancomycin
105.        How is Neisseria meningitides distinguished from other bacterial species we have discussed?
105.       Gram-negative, kidney bean-shaped, osidase-positive diplococcic
106.        What type of Virulence Factors does N. meningitides have?
106.       Pili, LPS, Polysaccharide capsules
107.        Where does N. meningitides reside in the body?
107.       nasopharynx
108.        What populations are at risk of contracting bacterial meningitis?
108.       Children ages 2-18, Adults in crowded conditions, alcoholism
109.        What organism is a small nonmotile gram-negative bacillus, that causes meningitis?
109.       Haemophilus influenza
110.        What are the 3 main causes of otitis media in children?
110.
1. Strep pneumo
      2. H. influenza
      3. Moraxella
111.        What treatment is used for otitis media?
111.       third generation cephalosporin with dexamethasone
112.        Why is dexamethasone used?
112.       to control inflammation
113.        How is Listeria monocytogenes usually contracted?
113.       foodborne
114.        How long did I spend studying Micro?
114.       To long for only 8 questions on the exam.
115. T/F: Penicillin is the drug of choice for treatment of a staphylococcal infection?
F
Virtually all strains of Staph carry bacterial plasmids encoding Beta-lactamases making them resistant to penicillin (therefore Pen is never the first choice)

Methicillins or 1st gen Cephalosporins are the first choice (assuming the strain is sensitive).

116. MRSA

Methacillin-resistant Staph aureus

;

A major problem!

MRSA have a unique penicillin binding protein that makes them resistant to methicillins, penicillins, and cephalosporins.

;

For serious MRSA infections tx w IV vancomycin Daptomycin is also effective against MRSA and VRE (Vanc-R enterococci), depolarizes bacterial membranes.

What type of infections is S. epidermis responsible for and how are these infections typically treated?
S. epi is the leading cause of mosocomial bacteremia (as a result of the use of IV catheters).

Is also the most common cause of prosthetic heart valve infections.

S. epi tends to be methicillin resistant which makes treatment difficult.
Vancomycin is typically used, sometimes in combination with rifampin or an aminoglycoside.

116. How do you distinguish S. saphrophyticus from S. epi?
S. saprophytic us is resistant to Novobiocin while S. epi is sensitive.
117. What is the most significant cause of CA-UTIs?
E. coli (by far)
but S. saphrophyticus (which is normal flora of the skin and periurethral areas) is the second leading cause of this infection.
118. Cystitis
An infection of the bladder, typically caused by bacteria (in which case it is called a UTI)

Symptoms: suprapubic pain, dysuria, frequency/urgency of urination, PMN in urine, significant bacteruria.
Typically not accompanied by fever*

If these symptoms exist without significant bacteruria, pt should be tested for STIs.

119. T/F: Sterptococcal species die in the presence of oxygen?
F. Strep species are aerotolerant, however, they are anaerobes.

Note that there is an exception to this (peptostreptococcus) which is a strict anaerobe important in wound infections. [will be discussed in the anaerobes lecture]

120. Name an example of a Group A streptococcal agent.
S. pyogenes
121. Name an example of a Group B streptococcal agent.
S. agalactiae
122. Name examples of agents which are grouped into Lancefield Group D

Strep bovis,

Enterococcus faecalis,

Enterococcus faecium

123. To which Lancefield group does S. pnumoniae belong?
None!
Strep pnumo is a non-typable alpha-hemolytic strep.
124. Name examples of alpha hemolytic streptococcal species.
Strep pneumo
Viridans strep

Note that most group A and B members are beta hemolytic, many non-typable strains (such as step pneumo and viridans) are alpha hemolytic and many group D members are gamma hemolytic.

125. Describe the polysaccride capsules of the following species:
S. pneumonia
S. pyogenes
S. mutans
S. pneumo (no group) has a capsule containing many different types of carbohydrates.

S. pyogenes (GAS): has a capsule containing a lot of Hyaluronic acid.

S. mutans capsule contains polydextrans that help it form dental plaques.

126. What is Protein A? Where is it found and what does it do?

Protein A is a major component of the bacterial cell wall.

It is also sloughed off of some bacteria and can be anti-phagocytic.

;

In S. aureus protein A is a MSCRAMM. It is recgonized (along with clumping factors A and B) on the surface of S. aureus in Latex Aggulutination Tests.

;

Protein A binds to the Fc portion of IgG and prevents activation of complement (anti-phagocytic property).

127. What two things are encoded for in the genomes of all G(+) bacteria?

1) MSCRAMMs

;

2) LPXTG Motif (a specific amino acid sequence that is cleaved by the enzyme sortase to attach the protien to uncrosslinked peptidoglycans to allow interaction with a host).

130. What type of infection(s) are Chronic Granulomatous Dz pt succptible to and why?

Staphlococcal infections.

;

Granulomatous Dz pts do not make ROS used to kill many types of bacteria.

Staph species are catalase positive which means they are able to break down the minimal amounts of hydrogen peroxide in the phagcytes of these pts leaving their phagocytes helpless to fight infection.

;

Strep infections do not present a problem to these pt because Strep is catalase negative.

131. What is another name for Coagulase?

Coagulase = Clumping Factor

;

A MSCRAMM found in S. aureus species.

132. What is a Thermonuclease Test and what is it used to determine?

Thermonucleases are DNases.

;

They are present in S. aureus but not in other forms of staph.

133. What are Panton-Valentine Leukocidins?

These leukocidis are capable of lysing PMNs and are found in most CA-MRSA.

These isolates cause particularily severe infections.

134. Describe the differences in growth charactaristics on BAP between Coag+ and Coag- staph strains.

Both can grow on blood agar plates and both are beta-hemolytic.

;

S. aureus produces golden-colored colonies while CoagNS typically produce white colonies.

135. Name some dz caused by Staphlococcal Exotoxins (ETs)

Stahplococcal Scalded Skin Syndrome (SSSS),

Staphlococcal Scarlet Fever (which is a generalized form of SSSS),

Bullous Impetigo (blisters)

136. T/F TSS is caused by Staph only

F.

Can be caused by Staph or Strep superantigens.

Specifically those of Staph aureus and Strep pyogenes.

137. Name some GAS MSCRAMMs

M protein is the most significant, although there are others (M-like protein, F1/2, Epa)

;

M protein is anti-phagocytic (either due to binding fibrinogen or C4b binding protien, either way inhbiting complement activation and thereby hindering phagocytosis).

;

M protein is implicated in the development of acute rheumatic fever.

;

anti-M abs are protective but there are multiple serotypes of M.

138. Explain the role of fimbriae in S. pyogenes virulence.

Fimbriae are a key mechanism of virulance for many species.

;

In GAS, fimbriae are made up of M protein (a MSCRAMM) and Lipoteicholic Acids (LTA, pro-inflammatory adhesins).

Both of these components contribute to its virulence.

139. What symptoms are streptococcal pyrogenic exotoxins (SPEs) responsible for?

The rash and fever associated with Scarlet Fever.

;

Streptococcal TSS

;

Necrotizing fasciitis pathogenesis.

;

Myositis

140. What are SLO and SLS responsible for and what is the difference between them?

SLO and SLS (Streptolysin O and S) are hemolysins responsible for beta hemolysis on a blood agar plate.

;

SLO is oxygen labile while SLS is oxygen stabile.

;

SLO is used to dx ARF.

141. How does S. pyogenes react to Bacitracin exposure?

S. pyogenes is Bacitracin Sensitive.

;

Bacitracin is used to distinguish Group A strep (BacitracinS) from Group B strep (Bacitracin R)

142. What is most commonly the cause of a sore throat?

VIRUSES*

;

If it is bacterial it is likely to be GAS but it is most likely viral.

(if it is GAS, tx with PenV)

143. What is Scarlet Fever? What causes it?

A dz caused by SPE+ (Strep pyogenic exotoxin) strains of S. pyogenes.

;

It is the toxin, rather than the strep itself which causes the symptoms (Strawbery tounge, red rash, sore throat, and fevers).

144. What causes Necrotizing Fasciitis and Myositis?

Can be a mono or polymicrobial infection!

;

In either case GAS and/or S. pyogenes can be involved (as can other organisms).

;

;

145. T/F ARF may follow a GAS skin infection

False.

GAS my follow strep throat but does not follow streptococcal skin infections.

146. Acute glomeruloneprhitis

May follow either a streptococcal pharyngitis OR a skin infection (unlike ARF).

;

Associated with speficic M proteins which are siad to be nephritogenic.

;

An immune complex dz

147. What is the key example we studied of GBS?

S. agalactiae (detectible by rapid group B carbohydrate latex agglutination test).


Beta-hemolytic, Bacitracin R, has multiple antiphagycitc cpasule types which contain sialic acid and are the major source of virulence for this GBS.


Normal flora of the GI and oropharynx but also colonize the vagina during pregnancy.

148. Name a disease caused by GBS

;Neonatial sepsis

;

Mothers now screened.

E. coli and some G- enterics also imporant.

Causes septicemia, respiratory distress, early onset after birth.

Can lead to meningitis and respiratory disease.

;

GBS can aslo cause infections, septicemia and endocarditis in immunocomprimised adults.

;

149. What are some of the defining charactaristics of Enterococcus species.

It is considered an “honorary strep”

G(+) cocci

;

All are Lancefield Group D (but some strep are also D)

;

Bile esculin +

Salt tolorant

Some resistance to heat (overall hardy)

;

Noraml folor of the skin, upper RT, GI and GU tracts.

;

Most dz caused by this group is by E. faecalis and E. faecium is the strain most frequently VancR (VRE)

150. T/F Enterococcus infections can be treated with Cephalosporins.

False.

;

Enterococcus species are naturally resistant to Pen and to Cephalosporins with some strains being Vancomycin resistant (VRE).

;

Some of the world’s most resistant bacteria are in this group!

151. Name 3 dz caused by Lancefield Group D species.

1. Nosocomial Infections (ex: UTI, septicemia, wound infection; Enterococci commonly involved in all)

;

2. Subacute endocarditis (SBE), particularily involving the valves (Enterococci)

;

3. Bacteremia: occurs when the colonic mucoas is disurpted by a tumor and S. bovis gets into to blood.

Is indication for a colonoscopy (intestinal cancer).

152. Vancomycin

A glycopeptide abx which inhbits crosslinking of NAM and NAG in PG cell wall formation.

;

Effective against G + species only.

;

Used to treat potentially debilitating/fatal Dz:

MethR Staph infections (though there are Vanc alternatives here),

Pneumococcal meningitis (empirical tx, bf sensitivity profiles get back from the lab),

C. difficile infections/psudomembranous enterocolitis (again, alternative options are avail.)

;

Always adjust tx when sensitivities are known.

;

153. What are some organisms that are VancR

;

VRE: VancR Enterococcus, typically E. faecium

(the original VancR organism)

;

VRSA: VancR S. aureus

(aquired resistance from Enterococcal species).

154. What drugs are used to tx VancR strain infections?

Linezolid is typically a first choice

;

Synercid (a combo quinupristin/daflopristin) + Streptogramns

[Inhibition of bacterial protein synthesis]

;

Daptomycin (lipoprotein that depoloarizes G+ bacterial cell walls causing bacterial cell death)

155. What classifies a specieis as a member of the Viridans group?

Viridans are a group of streptococci that excludes S. pneumo.

;

Are non-typable by Lancefield groups.

Alpha-hemolytic

;

Normal flora in the oral/pharyngeal cavities.

Important opportunists (SBE, bacteremia)

;

Notable member of this group: S. mutans has a slimy capsule of sucrose which allows it to attach to teeth and cause dental carries.

156. What causes dental carries?

S. mutans

;

Viridans group strep (alpha hemolytic)

157. What is the most common cause of Subacute bacterial endocarditis (SBE)?
Viridans group strep.

158. Streptococcus pneumoniae

Classification, identifying charactaristics, related illnesses.

Non-typable alpha hemolytic strep that is not (for some unknown reason) considered a part of the Viridans group.

Can be normal flora of the pharynx.

Lancet-shaped

Diplococci*

;

OptochinS

(used to identify it from other alpha-hemolytic strep species like S. viridans which are OptochinR)

Bile-soluble

(to distinguish from S. bovis and Enterococci which are not dissolved by bile).

;

Capsule of S. pneumo=major virulence factor

(Anti-phagocytic, basis of pnumo vaccines, detectible by rapid agglutination tests).

159. What is pneumolysin and why is it important?

Pnumolysin is a key virulence factor of Strep pneumo.

;

Can lyse cells by binding to membrane cholesterol and forming a pore.

160. How does S. pneumo cause dz?

S. pneumo establishes infection (in RT, lungs, meninges, blood) by escaping host natural and adaptive immune responses and inducing inflammation (has C-substance which binds to C-reactive protein, inducing the release of acute phase reactants=inflammation).

;

Ex: death from pneumonia is the result of an inflammatory response elading to excessive fluid accumulation in the lungs which causes suffocation.

161. Pneumonia

Cause(s), charactaristics/symptoms, risk factors.

Leading cause of bacterial pneumonia is Strep pneumo.

;

Is most common in the elderly.

;

Presents with a shaking chill (single rigor), rusty sputum (productive cough), pleuritic pain, and fever.

CXR shows lobar consolodation (due to fluid accumulation).

;

Risk Factors: recent viral infection, chronic pulmonary dz, splenic disorders (SSA, DM, asplenia).

162. How is pneumococcal pneumonia treated?

Variable resistance patterns make abx tx difficult.

Multiresistant Strep pneumo (MSRP) = problematic.

Sensitivies should be ordered for all isolates.

;

If sensitivity allows, tx with Pen or ceftriaxone (3rd gen cephalosporin).

;

In PenR strains, tx with a fluroquinone liek Levofloxacin (broad spectrum, high toxicity)

164. What is the best thing one can do to prevent pneumococcal pneumonia?

Prevent inflenza via flu vaccine!

;

Viral illness predisposes to pneumonia!

164. Other the pneumonia, what other illnesses can S. pneumo cause?

URI

(otitis media, sinusistis, conjunctivitis)

;

Septicemia

;

Meningitis

(S. pneumo is the leading cause of bacterial meningitis in adults)

165. What are the causes and symptoms of bacterial meningitis?

Causes: First weeks of life (GBS)

3 mo-18 yrs (Neisseria meningitis)

18-50+yrs (S. pneumo)

*Haemophilus, Listeria, E. coli are also causes.

;

Symptoms:Stiff neck, Headache, photophobia, fever, vomiting, neuro dysfunction.

;

CSF Findings: High opening pressure, large numbers of PMNs*, elevated protien levels.

;

If bacterial meningitis is suspected a combination of Cephalosporin and Vancomycin is often used (tx S. pneumo-caused meningitis).

166. T/F, one can be vaccinated against pneumonia?

True

;

Pneumovax is a non-conjugated vaccine for older people and those at high risk due to AIDS, asplenia, transplant.

Not effective in kids.

Protects against invasive pneumococcal dz.

;

Prevnar is a new, expensive but safe, conjugated vaccine effective in children as young as 2 mo, creates a memory response.

167. Nisseria meningitidis

Qualities/identifying charactaristcs and related dz.

G(-) *unique in this assessment material

Kidney-bean shaped

Diplococcal

Oxidase positive.

;

The most common cause of bacterial menigitis in children (3 mo-18 yrs); can have very rapid dz progression leading to death.

Also a cause of bacteremia (Meningococcemia)

Throat (normal flora) ; Blood ; Meninges

;

Virulence Factors: Pili, LPS, polysaccride capsule (distinguishes N. mengitidis from N. gonorrheae)

*Capsule is the basis for detection by rapid agglutination and for vaccine formulations.

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Risk Factors:Crowded populations and alcoholism, endemic in some areas.

;

While rapid tx is vital, resistance is not a huge problem with N. meningitidis infections.

;

168. A maculopaplar to petechial or pupuric skin rash (with fever, headache and neuro signs) indicates what type of infection?

Meningococcemia

(bacteremia caused by N. meningitidis)

;

Is more rare than bacterial meningitis caused by N. meningitidis.

;

While prompt tx is vital, resistance is not a huge problem with N. meningitidis.

169. T/F one can receive prophylaxis for N. meningitidis infections.

True

;

Ciprofloacin (floroquinalone abx which inhbits DNA synth) is given to those at high risk: colse contacts, medical personal etc…

170. Haemophilis influenzae (H. flu)

Identifying charactaristcs, related dz and prevention

;G- rod *unique in this assessment

Non-motile

Does not grow on BAP

(distinguishes from Strep/staph/enterococcus)

Does grow on Chocolate Agar Plate

(CAP, contains grwoth requirements for fussy bacteria)

;

Since the vaccine, the incidence of H. flu caused bacterial meningitis has plumeted (only now occurs in partially/unvaccinated infants).

;

Unencapsulated H. flu is a huge cause of otitis media in children (2nd behind S. pneumo)

Type b (the invasive type) has a capsule which allows it to cause severe systemic dz: meningitis, epiglottitis, cellulitis, osteomyelitis, pneumonia.

;

Tx: Ceftriaxone typically used to tx H. flu infections

AmpR is common.

;

Prevention: There is an effective conjugated type b vaccine that is part of standard vaccination series.

;

;

;

171. Listeria monocytogenes

Identifying charactaristics, sources of infection, and related dz.

G(+)

Club-shaped Rod

Motile over a ltd. temp range.

;

A facultative intracellular parasite that infects mucoasl epi cells and non-immune macropahges.

;

Sources: The environment (animals); human infection is typically food-borne (unpasturized cheeses, hot dogs, deli meat).

;

Dz: Uncommon but serious food-borne illness with req hospitalization and high mortality.

Infections are flu-like in normal adults and more prevalent in pregnant women.

Can also cause bacteremia, meningitis in the immunocomrimised and neonates.

172. An otherwise healthy 18 yo girl presents to the ED with a headache, altered mental status, neck stiffness and a high fever.

What are the first two things you do?

You suspect bacterial meningitis.

;

1) Take blood/CSF cultures (send off for succeptibilites)

;

2) Treat empirically

Cephtriaxone (broad spec abx, 3rd gen Cephalosporin)

+ Ampicillin (if listeria is suspected)

or + Vanc (if R S. pneumo is common in your area).

173. What are some causes of actue pharyngitis

Bacterial: GAS, N. gonorrhoeae

;

Many viral causes incl Rhinovirus/Coronovirus (common cold viruses) and Adnenovirus.

174. Name some agents of acute bronchitis (uncomplicated)

90% is caused by viruses and therefore should not be tx w/ Abx unless culture indicates.

;

Viruses: Coronavirus, Rhinovirus, adenovirus (URT)

Influenza (LRT)

;

Bacteria can cause more bronchitis in pt with underlying lung/respiratory problems*

S. pneumo, H. flu can cause in this case.

175. Tx of S. pneumo infections causing:

Acute Otitis Media (AOM)

Pneumonia

Meningitis

;

AOM: Amoxicillin

;

Pneumonia: Amoxicillin or PenG (if PenS)

High dose Pen or Cephtriaxone (if Pen intermediate)

Fluroquinilone [Linezolid or Synercid] (if PenR)

;

Meningitis: High dose PenG or Cephtriaxone (if PenS)

Vanc+Ceph (if PenR)

;

All S. pneumo are B-lactam resistant due to altered penicillin binding proteins (PBP) not due to beta lactamases*

;

All S. pneumo are VancS at this time.

176. Bile esculin/High Salt medium

Used to tell Group B strep and Enterococci apart from other Strep strains and from one another.

;

GBS is the only type of strep that can grow in a high-salt medium.

;

Enterococcal species can not only grow on this media but can convert bile esculin to a black breakdown product (distinguishing it from GBS).

;

;

177. What test is useful in distinguishing S. aureus from S. epidermis?

Thermonuclease Test

;

S. aurueus (but not other staph, incl. epidermis) produces a heat-resistant DNase (a thermonuclease).

;

Samples are boiled in blood broth culture and then inoculated on a thermonuclease plate.

;

If S. aureus was present in the original culture its thermonucleases will have survived the boiling and will turn the blue agar pink.

178. What test is useful in distinguishing S. pneumo from S. viridans?

Bile Solubility

;

S. pneumo contain autolysins that are activated by bile salts. When bile salts are dropped onto a S. pneumo culture the entire culture will autolyse and disappear!

;

Viridans and other species will persist.

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Categories: Microbiology