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PCM II Final > Bacteria > Flashcards

Bacteria Flashcards

1
Q

5 Morphologic characteristics of Staphylococcus aureus

A

Gram-positive cocci

Catalase+

Coagulase+

Beta-hemolytic

Mannitol fermenter (turns salt agar yellow)

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2
Q

Main virulence factor associated with Staph aureus — component of cell wall which binds Fc region of Abs and prevents complement activation thus preventing opsonization and phagocytosis

A

Protein A

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3
Q

What area of the body does Staph aureus tend to colonize?

A

Nares (nose)

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4
Q

What are the 5 inflammatory diseases caused by Staph Aureus?

A
  • Post-viral bacterial pneumonia (patchy infiltrate on CXR)
  • Septic arthritis (#1 cause)
  • Large erythematous abscesses
  • Rapid onset bacterial endocarditis (IV drug use, often tricuspid valve)
  • Osteomyelitis in adults (#1 cause)
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5
Q

3 morphologic features of Staphylococcus epidermidis and saprophyticus

A

Gram+

Catalase+

Urease+

Coagulase -

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6
Q

What morphologic feature differentiates Staphylococcus aureus from Staph epidermidis and saprophyticus?

A

Staph aureus is coagulase+

Epidermidis and saprophyticus are coagulase -

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7
Q

What organism is a part of normal skin flora and tends to infect hardware, orthopedic joints, heart implants, catheters, etc.?

What virulence factor contributes to its ability to do this?

A
  • Staphylococcus epidermidis
  • Polysaccharide capsule: ability to form biofilms to stick to metal and plastic surfaces
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8
Q

What organism is associated with contamination of blood cultures?

A

Staph epidermidis

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9
Q

What is the major clinical manifestation of staphylococcus saprophyticus?

A

UTI’s in sexually active females (2nd most common cause to E.coli) “Honeymoon cystitis”

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10
Q

Morphologic features of streptococcus pyogenes (group A strep)

A

Gram+ cocci in chains

Microaerophilic

Hyaluronic acid capsule

Beta-hemolytic

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11
Q

5 Virulence factors associated with S. pyogenes (Group A strep)

A

M-protein (anti-phagocytic, humoral response - Abs to heart)

Streptococcal pyrogenic exotoxin

Streptolysin O

Streptokinase

DNA-ase

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12
Q

Clinical manifestations of strep pyogenes infection (note which ones are toxin-mediated vs. M-protein mediated)

A

Pyogenic infections:

Impetigo, strep throat, erysipelas, cellulitis

Toxin-mediated:

Scarlet fever, TSLS, Necrotizing fasciitis

M protein-mediated:

Rheumatic fever = polyarthritis, endocarditis (mitral valve), nodules on extensor surfaces, erythema marginatum, sydenham’s chorea [JONES]

Post-streptococcal glomerulonephritis:

Facial edema, hematuria (“cola” colored urine), HTN

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13
Q

How would you test for a group A strep infection?

A

ASO antibody titer

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14
Q

3 symptoms of Scarlet fever?

Caused by what toxin?

A
  • Strawberry tongue
  • Pharyngitis
  • Widespread rash that spares the face
  • Caused by streptococcal pyrogenic exotoxin (SPE)
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15
Q

Which superantigens mediate TSLS vs. Necrotizing fasciitis in strep pyogenes infections?

A
  • TSLS = SpeA, SpeC
  • Nec Fasc = SpeB
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16
Q

Post-streptococcal glomerulonephritis tends to occur after what type of strep pyogenes infection(s)?

A

Either pharyngitis OR superficial infection like impetigo

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17
Q

Rheumatic fever tends to occur after what type of strep pyogenes infection(s)?

A

Pharyngitis only (NOT impetigo!)

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18
Q

What organism tends to cause serious infections in newborns, thus pregnant mothers should be swabbed at ~35 weeks?

A

Streptococcus agalactiae (group B strep)

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19
Q

Morphologic features of strep agalactiae and distinguishing tests?

A

Gram+ cocci in chains

Facultative anaerobe

Beta-hemolytic

Polysaccharide capsule

cAMP test + (increasing zone of hemolysis when plated w/ S. aureus)

Hippurate test +

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20
Q

Clinical manifestations of streptococcus agalactiae (Group B strep)

A
  • Neonatal meningitis (no nuchal rigidity!) = #1 cause
  • Strep throat (pharyngitis)
  • Pneumonia
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21
Q

Morphologic features of streptococcus pneumoniae?

A

Gram + diplococci

Polysaccharide capsule = major VF

Alpha-hemolytic

Facultative anaerobe

Optochin-sensitive

Bile-soluble

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22
Q

Characteristic feature of otitis media caused by streptococcus pneumoniae

A

Bullous meringitis

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23
Q

Major virulence factors of strep pneumoniae?

A
  • Polysaccharide capsule
  • IgA protease = allows colonization and invasion of mucosa!
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24
Q

Diagnosis of strep pneumoniae involves the ____ reaction, which turns blue in the presence of strep pneumo

A

Quelling

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25
Q

1 cause of what conditions?

Clinical manifestations of streptococcus pneumoniae?

A

1 cause of MOPS:

  • Meningitis
  • Otitis media
  • Pneumonia - often lower lobes, PMN-rich rust-colored sputum
  • Sinusitis
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26
Q

Morphologic features of streptococcus viridans?

How to distinguish from Strep pneumoniae?

A

Gram+ cocci in chains

Facultative anaerobe

Alpha-hemolytic

Optochin-resistant (allows to distinguish from S. pneumonia)

Bile-resistant (allows to distinguish from S. pneumonia)

No capsule! (allows to distinguish from S. pneumonia)

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27
Q

Major virulence factor associated with streptococcus viridans?

Allows it to do what?

A

Extracellular dextrans —> adheres to platelets, especially in damaged heart valves (i.e., most often mitral valve)

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28
Q

Clinical manifestations of streptococcus viridans?

A
  • Dental caries (strep mutans)
  • Subacute bacterial endocarditis (only affects previously damaged heart valve — usually mitral valve) - Strep Sanguineous
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29
Q

Morphologic features of S. bovis

A

Gram+ cocci in chains

Facultative anaerobe

Usually gamma-hemolytic

Grows on bile (Bile resistant)

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30
Q

Clinical manifestations of S. bovis

A

Same as enterococcus:

- Subacute bacterial endocarditis

  • UTI
  • Biliary tract infection
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31
Q

S. bovis has a strong affilitation with what type of neoplasm?

A

Colorectal neoplasms

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32
Q

Morphologic features of Enterococcus faecalis and faecium?

A
  • G+ cocci in chains
  • Facultative anaerobe
  • Usually gamma-hemolytic
  • Grows on bile and 6.5% NaCl
  • Hugely abx resistant (VRE), nosocomial infections
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33
Q

Morphologic features of Bacillus anthracis?

A

Gram+ rods in chains (unique!)

Protein capsule (poly-D-glutamate)

Aerobe (but can grow w/o O2 so is facultative anaerobe)

Spore-former

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34
Q

Differentiate the 2 toxins associated with bacillus anthracis

A

Lethal factor — protease exotoxin that stimulates macrophage release of TNF and IL-1B contributing to death

Edema factor — acts on adenylate cyclase to increase cAMP (intracellulary) —> massive edema (resists phagocytosis)

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35
Q

Complication of GI anthrax?

A

Necrosis of intestines –> vomiting, abdominal pain and bloody diarrhea

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36
Q

Characteristic lesion associated with cutaneous B. anthracis infection?

A

Black eschar with surrounding (ring) erythema

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37
Q

Describe pulmonary anthrax

Known as what disease?

X-ray finding and progression?

A
  • Caused by spore inhalation (wool sorter’s disease)
  • Nonspecific symptoms at first, progresses to mediastinal LNs —> MEDIASTINAL HEMORRHAGE

- Characteristic WIDENED mediastinum on CXR,

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38
Q

Characteristics of bacillus cereus?

Often seen in what condition, caused by?

A

Aerobic

Spore-forming

Motile

No capsule!

Food poisoning from reheating fried rice — vomiting and diarrhea (heat labile vs. heat stable toxin)

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39
Q

Oxygen-status of all clostridium species

A

Obligate anaerobes: cannot survive around O2

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40
Q

Morphologic features of Clostridium tetani

A

Gram+

Flagellated (H-Ag+)

Spore-forming

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41
Q

Describe tetanus toxin associated with Clostridium tetani and its MOA?

A
  • Tetanospasmin - released from vegetated spores at puncture site, travels retograde, goes from peripheral motor nerves to spinal cord.
  • Acts as a protease on SNARE, inhibiting GABA and Glycine (inhibitory NTs) —> muscle spasm (spastic paralysis)
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42
Q

Characteristic features of C. tetani infection

A
  • Spastic paralysis leading to rigidity
  • Rhesus sardonicus (lock jaw)
  • Opisthotonus (exaggerated arching of back)
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43
Q

Morphologic fefatures of clostridium botulinum

A

Gram+

Obligate anaerobe (flourishes inside canned foods)

Flagellated (H-Ag)

Spore-former

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44
Q

Clinical features of C. botulinum infection in adults and infants?

Early sx’s?

A

Adults: DESCENDING flaccid paralysis (only affects PNS), starts with diplopia, ptosis as initial symptoms

Infants: floppy baby syndrome

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45
Q

Pathogenesis of C.botulinum infection in adults vs. infants

A

Adults: ingestion of preformed toxin (once it has germinated in improperly canned food), toxin then inhibits ACh nerves — toxin is a protease that attacks SNARE protein

Infants: ingest honey that contains SPORES

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46
Q

Morphologic features of Clostridium difficile

A

Gram+

Spore former

Motile (H-Ag)

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47
Q

Describe the 2 exotoxins associated with C.difficile and what they cause.

A

Exotoxin A = binds brush border — inflammation, cell death, and watery diarrhea

Exotoxin B = disrupts cytokskeleton integrity, by depolymerizing actin — enterocyte destruction and necrosis —> yellowish grey exudate called pseudomembranous colitis

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48
Q

How is C. difficile definitively diagnosed?

A

Look for TOXIN via PCR assay of stool

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49
Q

Morphologic features of Clostridium perfringens

Where is it found and associated with?

A

Gram+

Spore former

Non-motile! (found in dirt and soil - associated with combat wounds and motorcycle accidents)

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50
Q

Diseases associated with Clostridium perfringens and their pathogenesis

A
  • Gas gangrene (myonecrosis) — crackling sound on palpation due to alpha-toxin lecithinase (phospholipase) that attacks PM leading to RBC hemolysis
  • Food poisoning — late-onset watery diarrhea — ingest spores which then germinate in gut
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51
Q

Morphologic features of Corynebacterium diphtheriae?

Transmitted how?

A
  • Gram+ rod, but non-spore forming
  • Club-shaped (VERY pleomorphic)

- Bacteriophage-derived toxin (MUST be lysogenized)

  • Facultative anaerobe
  • Catalase+
  • Aerosol transmission
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52
Q

Describe the Corynebacterium diphtheriae toxin MOA?

What must happen to the toxin for it to be active?

What are the clinical manifestations?

A
  • Must first be lysogenized by a temperate bacteriophage!
  • Acts by ribosylation — inhibits EF-2 to inhibit protein synthesis —> gray pseudomembrane formation over throat and tonsils
  • Can cause airway obstruction and “Bull’s neck” LAD
  • Other effects: myocarditis (A-V conduction block and dysrhythmia), local paralysis (starting in posterior oropharynx) d/t myelin damage
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53
Q

Diagnosis of C.diptheria requires plating on what media?

How would you differentiate toxic vs. nontoxic strains?

A
  • Swab membranes and plate on Tellurite and Loeffler’s agar/media
  • Differentiate strains based on Elek’s test
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54
Q

Morphologic characteristics of Listeria monocytogenes?

A

Gram+ bacilli

Beta-hemolytic

Motile via flagella (H-Ag) — “tumbling” motility

Catalase+

Facultative intracellular

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55
Q

Risks for contracting Listeria monocytogenes?

Prefers what type of enviornment?

A
  • Can survive in cold environments — contaminates refrigerated items like milk and soft cheeses

- Pregnant women at risk - may lead to termination or disease in newborn, can give baby meningitis (meningitis also occurs in elderly with this)

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56
Q

What major VF allows L. monocytogenes to escape the phagolysosome?

A

Listeriolysin O

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57
Q

What conditions are associated with Moraxella catarrhalis infection?

A
  • Otitis media in pediatric patients (<3 y/o)
  • COPD exacerbations
  • URIs in elderly
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58
Q

Morphologic features of Neisseria

A
  • Gram-negative diploccoci
  • Oxidase+
  • Grows on chocolate agar, does NOT grow on blood agar
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59
Q

Since Neisseria cannot be grown on plain blood agar, what are the culture requirements for plating Neisseria?

A

Chocolate agar (heated blood agar)

VPN agar (Thayer Martin) = selective agar

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60
Q

Virulence factors associated with Neisseria?

A

Pilli — allow attachment to mucosa, antigenic variation

IgA protease — facilitates survival on mucosal surfaces Opa proteins

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61
Q

Which species of Neisseria is encapsulated (polysaccharide)?

How is it transmitted?

Where does it colonize first?

A
  • Neisseria meningiditis
  • Spread by respiratory droplets — first colonizes nasopharynx
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62
Q

Neisseria meningiditis ferments ____ and ______.

Most infections are caused by type _____ because it is not included in the vaccine.

_____ patients are at increased risk for this disease

A
  • Glucose; maltose (only meningitidis ferments)
  • Type B
  • Asplenic and sickle cell
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63
Q

Neisseria meningitidis invades hematogenously leading to a massive immune response generated by what?

Leads to?,

A
  • LOS proteins in envelope, which bleb off — causes inflammatory response –> increased permability –> leaky capillaries and hypovolemia
  • Petechial rash indicative of thrombocytopenia (can lead to DIC) —> eventual hypovolemic shock
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64
Q

What is Waterhouse-Fridrichson syndrome?

Occurs due to infection with?

A

Occurs with Neisseria meningiditis — characterized by hemorrhage/infarction of adrenals

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65
Q

Morphologic features of Neisseria gonorrhoeae?

Ferments what?

A
  • Gram-negative cocci
  • Facultative intracellular (likes to infect PMNs)
  • Note that it is NOT encapsulated,
  • Only ferments glucose (unlike N.meningiditis which is encapsulated and ferments glucose+maltose)
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66
Q

Clinical manifestations in N.gonorrhoeae in males vs. females?

Can spread to the perineum and form?

Manifestations in the infant?

A

Males: urethritis, white purulent discharge —> prostatitis, orchitis

Females: can cause PID —> purulent white THICK discharge, scarring, infertility, ectopic pregnancy,

Fitz-Hugh Curtis syndrome (violin string adhesions on liver) = PID spread to peritoneum

Both may exhibit polyarthritis (knees, often ASYMMETRIC)

Note that it can also be passed to baby during delivery causing early onset conjunctivitis (5-7 days after birth)

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67
Q

Fast vs. slow lactose fermenters?

A

Fast: Klebsiella, E.coli, Enterobacter

Slow: Citrobacter, Serratia

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68
Q

What 3 bacteria are urease+?

A

1) Klebsiella pneumoniae
2) Proteus mirabilis
3) Helicobacter pylori

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69
Q

Which 2 bacteria exhibit the following diarrheal manifestation:

Lack of cell wall invasion — entertoxin release leads to watery diarrhea

A
  • ETEC
  • Vibrio cholerae
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70
Q

Which 3 bacteria exhibit the following diarrheal manifestation:

Invasion of intestinal epithelium — adhere, invade, toxin release —> system response results in local WBC infiltraton (leukocytes in stool), fever, and cell death causing blood diarrhea

A

Enteroinvasive E. coli (EIEC)

Shigella

Salmonella enteriditis

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71
Q

Which 3 bacteria exhibit the following diarrheal manifestation:

Invasion of lymph nodes and bloodstream — WBC, RBC, abdominal pain; systemic response can lead to sepsis and bacteremia

A

1) S. typhi
2) Y. enterocolitica
3) C. jejuni

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72
Q

Describe characteristics of Enterobacter cloacae?

Ferments what?

Causes what infections?

A

Part of normal flora - cause pneumonia, UTI (multi-drug resistant nosocomial infections)

Ferments lactose (forms pink cultures on MacConkey agar)

Motile

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73
Q

Describe characteristics of Serratia marcescens infection?

Morphologic and lab characterisitcs?

A
  • Often infects wounds, causes pneumonia, UTIs (multi-drug resistant nosocomial infections)
  • Catalase positive
  • Very motile
  • Red pigment on culture
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74
Q

Klebsiella pneumoniae is an enteric with the potential to cause pneumonia, UTI, etc. and like other enterics, ferments lactose. What are the other morphologic features of Klebsiella?

A

Polysaccharide capsule (O-Ag)

Immotile (unique!)

Urease+

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75
Q

Characteristic findings for someone with a Klebsiella pneumonia?

What is seen on CXR?

A
  • Bulging fissure on CXR
  • Currant jelly-thick sputum
  • Cavitary lesions — may originally suspect Tb
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76
Q

Morphologic features of Salmonella typhi and enteritidis?

Grows on what agar and appears how?

A

Gram-negative bacilli - non-lactose fermenter

Motile (H-Ag) and Capsule (Vi Ag)

Produces H2S —> black colonies on Hektoen agar

Acid labile - easily degraded by stomach

Faculatative intracellular (in macrophages)

77
Q

Where would you find S. typhi in chronic carriers?

A

Gallbladder

78
Q

1 cause of what?

Clinical features of Salmonella typhi infection?

A
  • Rose-colored macules on abdomen
  • Osteomyelitis in pts with sickle cell (#1 cause)
  • Pea soup-diarrhea
79
Q

Morphologic features of Salmonella enteriditis?

Has what to increase infectivity?

A

Gram-negative bacilli and non-lactose fermenter

Motile

Produces H2S —> black colonies on Hektoen agar

Encapsulated (Vi antigen)

Acid-labile

Facultative intracellular (within macrophages)

Type III secretion system to increase infectivity

80
Q

Clinical features of Salmonella enteriditis?

Acquire infection how?

A
  • Acquired by eating undercooked chicken
  • Causes inflammatory diarrhea
81
Q

How would you differentiate Shigella from Salmonella infection in terms of plating?

A

- Green colonies on Hektoen agar INDOLE POSITIVE (Salmonella colonies are black)

82
Q

Morphologic features of Shigella?

Transmission?

Which cells take this organism up once inside intestine?

A
  • Gram-negative bacilli, unencapsulated, Acid stable
  • NON-motile
  • NO lactose fermentation and NO H2S production
  • Fecal-oral transmission
  • Taken up by M cells
  • Type III secretion system
83
Q

MOA of shiga toxin?

A

Inhibits 60s portion of ribosomes — inhibits protein synthesis and killing intestinal epithelial cells (bloody diarrhea)

84
Q

Clinical manifestations of Shigella infection

A
  • Causes bloody diarrhea (inflammatory containing RBCs and WBCs)
  • Damages endothelial cells within glomerulus, which activates platelets and causes aggregation –> thrombocytopenia
  • Shiga toxin may cause hemolytic uremic syndrome (HUS) in young patients (most common under 10 y/o) —> glomerular damage, thrombocytopenia
85
Q

Morphologic characteristics of E.coli?

Seen how on EMB agar?

A

Gram-negative bacilli

Catalase+

Facultative anaerobic

Lactose fermenter (pink MacConkey agar)

Siderophore

Indole+ (Green on EMB agar)

Encapsulated (K-Ag) and Flagella (H-Ag)

86
Q

Which type of E.coli infection is often derived from undercooked meat and causes bloody diarrhea, and is also the only E.coli that does not ferment sorbitol?

A

EHEC

87
Q

Describe the toxin associated with EHEC?

What strain is associated with outbreaks?

A
  • Shiga-like toxin — causes hemolytic uremic syndrome (HUS) and hemorrhagic colitis
  • O157:H7 Ag associated with outbreaks
88
Q

Describe the illness and toxin associated with ETEC?

Caused by what toxins?

A
  • Traveler’s diarrhea from drinking contaminated water - causes watery diarrhea
  • Heat labile —> increased cAMP (similar to cholera toxin)
  • Heat stable —> increased cGMP
89
Q

Characteristics of Yersinia enterocolitica infection?

Whom does it commonly affect?

Found where and transmitted via?

Morphological characteristics?

A
  • Found in puppy feces and milk products — commonly affects toddlers leading to bloody diarrhea, fever, leukocytosis
  • Resistant to cold temps (similar to Listeria)
  • Gram negative bacilli
  • Bipolar (safety pin) staining
  • Encapsulated
90
Q

Which bacterial infection can mimic an appendicitis?

A
  • Salmonella typhi
  • Yersinia enterocolitica
91
Q

Characteristics of Yersinia pestis; causes what?

Reservoir and vector?

How does it inhibit phagocytosis?

A
  • Reservoir = rodents and vector = fleas
  • Bubonic plague —> buboes (LAD)
  • Endotoxin—> necrosis of tissues and abscesses of organs
  • Yersinia outer proteins (YOPs) secreted via type III secretion system, inhibit phagocytosis
92
Q

Characteristics of Campylobacter jejuni?

Main reservoir?

Transmission?

A
  • Thermophilic (prefers warm temps)
  • Curved gram-negative rod
  • Oxidase+
  • Main reservoir = intestinal tract of animals (poultry)
  • Fecal-oral transmission; contaminated water or ingestion of raw milk
93
Q

Clinical manifestations of Campylobacter jejuni?

Post-infection complication?

A
  • Bloody diarrhea, bacteremia d/t invasiveness, reactive arthritis (Reiter’s syndrome)
  • Post-complication = Guillain Barre —> ascending paralysis
94
Q

Characteristics of Bacteroides fragilis

A

Gram-negative bacillus

Anaerobic

Normal flora of GI tract

NO lipid A!

95
Q

Clinical manifestations of Bacteroides fragilis?

May complicate what?

A
  • Secondary infection following abdominal trauma and/or localized abscesses
  • May complicate abortion, tubo-ovarian abscess, IUD
96
Q

Clinical manifestations of Bacteroides melaninogenicus and fusobacterium?

A
  • Melaninogenicus - can cause a necrotizing anaerobic pneumonia, following- GI aspiration; may also exhibit pneumonic and periodontal manifestations
  • Fusobacterium may have similar disease manifestations and rarely the etiology of otitis media
97
Q

Characteristics of vibrio cholerae, parahemolyticus, and vulnificus?

Endemic where?

Grows on what medium?

A
  • Gram-negative bacillus
  • Endemic to developing countries (SE Asia)
  • “Comma” shaped, grows on alkaline medium (acid labile)
  • Oxidase+
98
Q

Transmission and clinical manifestations of V**ibrio cholerae?

A
  • Fecal-oral transmission via contaminated food/water
  • Causes profuse watery diarrhea (“rice water” stool)
99
Q

Main virulence factor and pathogenesis of V**ibrio cholerae?

A
  • Fimbriae attach to intestinal wall and cholera toxin is released —> increased cAMP —> secretion of water and Cl- into lumen [other virulence factors: mucinase, motile via H-Ag]
100
Q

What 2 bacteria are at high risk of transmission via contaminated seafood, typically oysters?

Which causes Acute gastroenteritis?

Which causes fulminating septicemia leading to death?

A
  • Vibrio parahemolyticus –> fulminating septicemia –> Death
  • Vibrio vulnificus –> Acute Gastroenteritis
101
Q

Morphologic characteristics of Helicobacter pylori?

Major virulence factor?

Strains expressing which toxin allows them to better colonize the gastric body?

A
  • Curved Gram-negative bacilli
  • Motile (allows them to move through viscous mucus)
  • Oxidase+
  • Urease+ = major VF (important for reducing acidity of environment)
  • CagA expressing strains can effectively colonize the gastric body and cause multifocal atrophic gastritis
102
Q

Clinical manifestations of H.pylori?

Increased risk for what cancers?

How is it transmitted?

What part of the stomach are they most often found?

A
  • Duodenal ulcers (causes 95% of duodenal ulcers)
  • Fecal-oral transmission
  • Increased risk of gastric adenocarcinoma, MALTomas
  • Most often found in the antrum
103
Q

Morphologic characteristics of Pseudomonas aeruginosa?

Produces what pigment?

Distinguishable odor?

A
  • Gram-negative rod, obligate aerobe
  • Oxidase+
  • Catalase+
  • Encapsulated
  • Produces pyocyanin and pyoverdin —> blue/green pigment
  • Fruity grape odor
104
Q

What distinguishes psuedomonas aeruginosa from other enterics?

Thrives in what enviornments?

A
  • It is an obligate aerobe while most others are facultative anaerobes
  • Thrives in acquatic enviornments, hot tub folliculitis
105
Q

1 cause of?

Clinical manifestations of P**seudomonas aeruginosa?

Affects patients with CF, IV drug users, and diabetics how?

(Hint: mnemonic BE PSEUDO)

A
  • Complication of Burns
  • Endocarditis (frequently right herat valve in IV drug abusers)
  • Pneumonia (#1 cause of gram-negative nosocomial pneuomina; CF pt’s and immunocompromised)
  • Sepsis (infected catheters)
  • External malignant otitis media
  • UTIs (nosocomial)
  • Diabetic Osteomyselitis (IV drug users and children develop seconary to puncture wounds of foot)
106
Q

What is the pseudomonas toxin?

MOA?

What is it similar to?

A

- Exotoxin A is similar to Diphtheria toxin

  • Inactivates EF-2 by ribosylation; leads toinhibition of protein synthesis
107
Q

Characteristics of P**roteus mirabilis?

Characteristic odor?

May cause what type of infection?

A
  • Gram-negative rod
  • Urease+
  • H2S+
  • Facultative anaerobe
  • Swarming motility, may have fishy odor
  • Staghorn calculi
  • May cause UTI
108
Q

Proteus mirabilis cross-reacts with what other bacterial species?

A

Rickettsia

109
Q

Characteristics of Bordetella pertussis?

How does it cause infection?

A
  • Gram-negative rod
  • Filamentous hemagglutinin pilus attaches to ciliated epithelial cells of the bronchi and releases toxins
110
Q

Pathogenesis of Bordetella pertussis toxins?

A
  • Pertussis toxin: Ribosylates Gi (disabling it) —> increased cAMP
  • Adenylate Cyclase toxin: Increases cAMP [same MOA as edema factor]
  • Increased cAMP disables chemokine receptor for lymphocytes, leading to Lymphocytosis (increased WBC)

- Tracheal toxin: Damages ciliated cell in respiratory epithelium

111
Q

Clinical findings associated with Bordetella pertussis?

Describe each stage/phase.

During which stage is the disease most contagious?

A

1) Catarrhal stage: lasts from 1-2 wks of nonspecific findings including low-grade fever, conjunctival injection (red eyes), lacrimation, and mild cough
- Disease is most contagious during this stage
2) Paroxysmal stage: fever subsides and pt’s develop the characteristic cough - intense bouts of nonprodutive forceful cough, can last 2 weeks - 2 months
3) Convalescent phase: attacks becomes less frequent w/ a gradual reduction in symptoms; can last up to 3 months

112
Q

Characteristics of Haemophilus influenzae?

What is special about the medium needed to plate it?

VFs?

Transmission?

A
  • Gram-negative rod (coccobacilliary shape)
  • Grown on chocolate agar with factor V (NAD+) and X
  • VFs = Pilli, IgA protease, capsule (6 types)
  • Aerosol transmission
113
Q

Clinical manifestations of encapsulated Haemophilus influenzae

A
  • Epiglottitis: inspiratory stridor, drooling, “cherry-red epiglottis”
  • Otitis media
  • Meningitis (type B capsule only - most virulent)
  • Sepsis (most common in asplenic or sickle cell patients)
  • Septic arthritis in infants
114
Q

Clinical manifestations of nonencapsulated Haemophilus influenzae

A

Lack of invasiveness, so just causes COPD exacerbations, otitis media, and sinusitis

115
Q

Clinical manifestations of Haemophilus ducreyi

Transmitted how?

A

Chancroid (STI) — painful genital ulcer rapid, unilateral painful inguinal LAD

116
Q

Morphologic characteristics of Legionella pneumophilia?

How to visualize?

Needs what to grow on plate?

How is it transmitted?

A
  • Gram-negative rod, but needs silver stain to be visualized
  • Oxidase+
  • Charcoal yeast with cysteine and iron for plating
  • Facultative intracellular (inside amoebas)
  • Aerosolized contaminated water is inhaled (i.e., air conditioners, produce mist machines, and shower heads)
117
Q

How are infections with Legionella pneumophilia diagnosed?

A

Rapid urine Ag test

118
Q

Clinical manifestations of the 2 types of infections with Legionella pneumophilia

A

1) Legionnaire’s disease — more common in smokers; atypical pneumonia with unilobar patchy infiltrate, hyponatremia, headache, confusion, diarrhea, high fever (>104 F)

2) Pontiac fever — headache, myalgias, and malaise, followed by fever and chills - more self-limited

119
Q

Morphologic characteristics of Bartonella henselae?

How to visualize?

A
  • Gram-negative rod (zoonotic)
  • Warthin starry silver stain
120
Q

What diseases are caused by Bartonella henselae and what are their clinical features?

A

Cat-scratch disease: fever, painful regional LNs - axillary lymphadenitis, occurs in immunocompetent

Bacillary angiomatosis: also transmitted by cat scratches, occurs in immunocompromised (HIV) — fever, chills, HA, raised red vesicular lesions (similar to Kaposi sarc)

121
Q

Characteristics of Brucella?

Found where and trasnmitted how?

A
  • Gram-negative rod (zoonotic)
  • Found in farm animals
  • Direct contact w/ infected animal meat or ingestion of infected dairy products
  • Facultative intracellular in macrophages
122
Q

Clinical features of Brucella infection?

Characteristic of this infection?

A

- UNDULATING fever (characteristic), chills, anorexia, backache, and headache

  • Since it colonizes macrophages, it causes hepatosplenomegaly and LAD
123
Q

Characteristics of Francisella tularensis?

Vector and rervoir?

Why is this bacteria so dangerous?

A
  • Gram-negative rod (coccobacilli)
  • Encapsulated (antiphagocytic)
  • Facultative intracellular in macrophages
  • Vectors: ticks and deerfly
  • Reservoirs: rabbits, squirrels
  • POTENTIAL BIOTERRORISM AGENT — one of the most infectious pathogenic agents
124
Q

Clinical features of infection with Francisella tularensis?

Can have a presentation similar to what other disease?

A

- Ulceroglandular tularemia — Painful ulcer with black base (center with caseating necrosis), fever, LAD, systemic symptoms

  • Symptoms almost identical to bubonic plague

- Pneumonia tularemia — high mortality rate; via inhalation or through blood. Severe atypical pneumonia

125
Q

Morphologic features of Pastuerella multicoda?

Where is it found normally?

A
  • Gram-negative rod
  • NOT facultative intracellular: part of normal oral mucosa flora of domestic (i.e., cats/dogs) and wild animals
  • Catalase+
  • Oxidase+
  • Sheep’s blood agar
  • Encapsulated -
  • Bipolar staining (safety pin) - like yersinia
126
Q

Clinical features of Pasteruella multicoda infection?

How is it most commonly transmitted?

A
  • Cellulitis within 24 hours of bite; may progress to osteomyelitis
  • Most frequent wound infection following a cat or dog bite
127
Q

What differentiates Pasteurella multicoda from other zoonotics?

A

It is NOT facultative intracellular

128
Q

Morphologic features of Mycobacterium tuberculosis?

Transmitted how?

A
  • Acid-fast (mycolic acid in cell wall) - stains red
  • Carbol fuscin stain
  • Slow growing on Loenstein-Jensen medium
  • Obligate aerobe
  • Facultative intracellular (macrophages)
  • Transmission via inhalation
129
Q

Virulence factors of Mycobacterium tuberculosis?

A
  • Cell wall has glycolipids allows for clumping of bacteria into serpentine formation called cord factor.
  • Cord factor protects from destruction by eliciting caseating granulomas (tubercles) by increasing TNF and other cytokines, which activate macrophages
  • Sulfatides prevent phagolysosome fusion
130
Q

Clinical features of Mycobacterium tuberculosis primary infection?

What are the 3 outcomes of primary infection?

A
  • Healed primary infection affects lungs (usually lower or middle lobe), lesions become fibrotic and eventually calcify as do draining LNs, together forms Ghon complex = hilar lymphadenopathy + peripheral granulomatous lesion in middle or lower lung lobe

3 outcomes:

1) Healed latent infection —> fibrosis and + PPD (type IV HSR)
2) Systemic infection (miliary Tb) —> fulminant multiorgan failure
3) Reactivation Tb —> d/t immunosuppression —> TNF activation; affects upper lobes leading to hemoptysis, night sweats (classic sx), Pots disease, meningitis, tuberculoma

131
Q

Characteristics of Mycobacterium avium complex; how is it acquired?

Who does it affect most often?

Causes what?

A
  • Acquired from environment
  • Key player for immunocompromised
  • AIDS pts with CD4 <50, elderly smokers
  • Causes nodularities and bronchiectasis in middle aged non-smokers
  • Lymphadenitis in kids
132
Q

Characteristics of Ureaplasma urealyticum?

Causes what?

A
  • Pleomorphic, no cell wall, requires cholesterol, urease (+)
  • Non-gonococcal urethritis: burning dysuria, yellow mucoid urethral discharge
133
Q

Characteristics of Mycobacterium leprae?

Main reservoir?

Thrives in?

A
  • Acid-fast (carbol fuscion stain)
  • Non-motile
  • Facultative intracellular
  • Mycolic acids in cell wall
  • Thrives in cool temps
  • Main reservoir: armadillos
134
Q

What are the 2 clinical presentation(s) with Mycobacterium leprae infection and the features of each

A

Tuberculoid: Th1 cell-mediated — macrophage-contained; well-demarcated skin plaque; localized superficial, unilateral skin and nerve involvement

Lepromatous: Th2 cells, but no cell-mediated response. Not contained in macrophages and high chance of human-human transmission.

  • Glove/stocking neuropathy, lesions onextensor surfaces, profound facial deformity (leonine facies),saddlenose deformity, and internal testicular damage (leading toinfertility)
135
Q

Characteristics of Borrelia burgdorferi?

Vector, reservoir and obligatory host?

A
  • Spirochete
  • Microaerophilic
  • Wright stain and Giemsa stain + ELISA and Western blot (CMMRS)

- Ixodes tick is vector; reservoirs are mice, obligatory hosts are deer

136
Q

Clinical features of Borrelia burgdorferi infection?

Describe each stage.

A
  1. Early localized stage: Erythema chronicum migrans (bullseye rash), fever, chills
  2. Early disseminated stage: mutliple smaller ECMs, Heart block (myocarditis), bilateral Bell’s palsy, brief attacks of arthritis of large joints (knee)
  3. Late stage: chronic arthritis, encephalopathy

*Lyme Disease

137
Q

Characteristics of Leptospira interrogans?

Endemic where?

Where is it found and how do people get infected?

A
  • Spirochete - “Ice tong” or “question mark shaped”
  • Aerobic
  • Endemic in tropical areas (i.e., Hawaii)
  • Found in water contaminated with animal urine; associated with water sports
138
Q

Clinical features of Leptospira interrogans infection.

Describe each phase?

What is the severe illness it may cause?

A

1) Leptospiremic phase:bacteria invade thebloodandCSFand causeabrupt onsetofhigh fever, headache, malaise, and severe myalgias; classically theconjunctiva are redand pt hasphotophobia
2) Immune phase:appearance ofIgM Ab,pts may develop meningismus; CSF exam reveals anelevated WBC count
- Weil’s disease: or infectious jaundice, involving renal failure, hepatitis w/ jaundice, mental status changes, and hemorrhage in many organs

139
Q

Characteristics of Treponema pallidum

How is diagnosis of infection made?

Transmitted?

Reservoir?

A
  • Spirochete
  • Dark field microscopy needed for direct visualization
  • Use VDRL or RPR (non-specific) followed by confirmatory FTA-Ab test (specific)
  • Reservoir = humans (only)
  • Sexually (STD) –> Causes syphilis
140
Q

Clinical manifestations of adult syphilis; primary and secondary.

A

Primary: painless genital chancre (skin ulcer) erupts 3-6 weeks at site of inoculation; chancre is firm, ulcerated painless lesion w/ a punched-out base and rolled edges; resolves over 4-6 weeks

Secondary: untreated patients enter the bacteremic stage after about 6 weeks, becomes systemic: maculopapular rash on palms/soles within weeks to months, condyloma latum (wart-like lesions) on mucous membranes (i.e., vulva and scrotum); generalized LAD, weight loss, fever and almost any organ can be affected

141
Q

Clinical features of congenital syphilis

A
  • Anterior bowing of tibia (saber shins)
  • Saddle nose
  • Hutchinson teeth and Mulberry molars,
  • Deafness,
  • Widespread rash, rhinitis, and hepatosplenomegaly (characteristic of early congenital syphilis)
142
Q

What is the Jarisch Herxheimer rxn?

A

When you first treat syphilis with penicillin, symptoms may worsen prior to improving — fever, chills, HA

143
Q

Characteristics Chlamydia trachomatis

A
  • Gram-negative obligate intracellular
  • No peptidoglycan or muramic acid (cannot grow on media)
  • Giemsa stain to visualize
  • Dx with NAAT test (PCR)
  • Exists in 2 forms: Elementary body and Initial body
144
Q

Clinical features of 3 groups of Chlamydia trachomatis

Is the most common and leading cause of what?

A

A-C: Blindness (leading cause worldwide!) - *A-B-SEE*

D-K: characteristic watery discharge, cervicitis, epididymitis, PID, neonatal transfer—> conjunctivitis, pneumonia (most common STD)

L1-L3: lymphogranuloma venaerum - painless genital ulcer, tender LAD in inguinal region

145
Q

Complications of C. trachomatis infection

A

- Reactive arthritis (Reiter’s syndrome) “Can’t see, can’t pee, can’t climb a tree” — conjunctivitis, urethritis, arthritis

- Fitz Hugh Curtis syndrome (perihepatitis): infection of liver capsule w/ sx’s of RUQ pain

146
Q

Clinical features of Chlamydia pneumoniae and psittaci?

How are they transmitted?

A

Pneumoniae species is TWAR; causes atypical pneumonia in young adults; transmitted via respiratory route

Psittaci causes pneumonia 1-3 weeks after exposure; transmission by bird droppings or dust from feathers (think parrots, vets, and workers in poultry slaughterhouse or pet-shop)

147
Q

Characteristics Coxiella burnetti

Reservoir and transmission

What does it cause and the classic findings?

Complications caused by this infection?

A
  • Gram negative rod
  • Obligate intracellular
  • Contained in spores in animal poop (resistance to heat, exists extracellularly, and non-arthropod transmission)
  • Aerosol transmission
  • Causes Q fever — abrupt onset of fever, soaking sweats, headache, viral-like pneumonia (cough), w/ NO RASH!

- Complication: granulomatous hepatitis and culture negative endocarditis

148
Q

Clinical features of Gardnerella vaginalis?

What are the classic signs and how is it diagnosed?

A
  • Gram negative bacillus that causes bacterial vaginosis (bacterial overgrowth of normal anaerobic flora creates a suitable enviornment for growth Garnerella)
  • Burning, pruritis (itching) of labia, dysuria (burning), and a copious, foul-smelling vaginal discharge w/ fishy odor
  • Dx via KOH whiff test or Clue cells (epithelial cells coated in bacteria)
149
Q

Characteristics of Mycoplasma pneumoniae

What is seen on CXR?

A
  • NO cell wall - won’t gram-stain
  • Grows on Eatons agar
  • Only bacteria with CHOLESTEROL in cell membrane
  • CXR reveals streaky infiltrate, which usually looks worse than the clinical sx’s and PE suggests
150
Q

Clinical features of Mycoplasma pneumoniae infection?

Who’s most often affected?

Diagnosed how?

Associated with what other pathologies?

A
  • Causes “walking pneumonia” with patchy infiltrate and tracheobronchitis
  • Increased incidence in young adults and military recruits - close quarters
  • Dx via cold agluttinins (clumped RBCs in cold temps) - IgM, may also see bullous meringitis on PE
  • Associated with erythema multiforme and Steven Johnson syndrome
151
Q

General Rickettsia morphology

Tropism for?

Diagnose how?

A
  • Gram-negative (coccobacillary) but doesn’t stain well (pleomorphic)
  • Obligate intracellular
  • Tropism for endothelial cells that line blood vessels
  • Unable to produce NAD or CoA; rely on eukaryotic cells
  • Dx with Weil Felix agglutination test; Cultiure: chick yolk sac; Serology
152
Q

Clinical features of early undetermined Rickettsia infection?

A

Prodromal headache and fever, vasculitis/rash

153
Q

Clinical features of Rickettsia prowazekii infection?

How is it transmitted?

What type of Typhus?

A
  • Rash starting on trunk and spreading to extremities, SPARES hands/feet; myalgia, arthralgia, encephalitis, dizziness, confusion, coma
  • Affects military recruits and POWs
  • Spread by louse poop that gets into scratches
  • Causes EPIDEMIC typhus (OX-19) — widespread rampant outbreak
154
Q

Clinical features of Rickettsia rickettsii infection

How is it transmitted and what is the reservoir?

Weil-Felix Ag findings?

A
  • Rocky Mtn Spotted Fever, OX-19, OX-2 (Weil-Felix Ags)
  • Transmission via dermacentor ticks (wood or dog ticks)
  • Reservoir = dogs, rabbits and rodents
  • Rash takes 2-14 days to develop, extends from extremities —> centrally; headache, fever, myalgias
155
Q

Clinical features of Rickettsia akari infection?

Weil-Felix Ags?

Reservoir and transmission?

A
  • Rickettsial pox: mild, self-limiting fever; blister at bite site then vesicular rash and headache — Weil Felix NEGATIVE
  • Reservoir = house mice
  • Transmission = mites (live on house mice)
156
Q

What condition is very similar to Rocky Mtn Spotted Fever but is NOT associated with a rash?

A

Erlichiosis

157
Q

A male smoker presents with pneumonia, high fever, diarrhea, hyponatremia, and neurological symptoms, including headache and confusion.

What organism and disease do you suspect?

Gram positive or negative?

A

Legionella (Gram negative) –> Legionnaire’s Disease

158
Q

How is Francisella tularensis transmitted?

Main reservoir for this bacteria?

Other modes of transmission?

A
  • Transmitted via Dermacentor tick
  • Main reservoir = rabbits
  • Can be aerosolized and potentially used in bioterrorism
159
Q

Once Francisella tularensis is acquired what occurs?

A
  • Causes painful ulcer
  • Macrophages pick it up and travel through lymph system to the reticulo-endothelial organs
  • Causes granulomas w/ caseating necrosis in the reticulo-endothelial organs (spleen, liver, and LNs)
  • Regional lymphadenopathy
160
Q

What type of bacteria is Francisella tularensis?

A

Gram negative coccobacilli

161
Q

What type of bacteria is Pasteurella multocida?

Positive lab tests?

Grows well on what agar?

Demonstrates what staining?

A
  • Gram negative
  • Oxidase positive
  • Catalase positive
  • 5% sheeps blood agar
  • Bipolar staining (safety pin staining)
162
Q

Main reservoir for Pasteurella multocida?

How is it transmitted?

Virulence factor?

A
  • Respiratory tract of small animals - Dogs and cats
  • Transmitted via dog and cat bites
  • Capsule is its VF
163
Q

What occurs after infection with Pasteurella multocida?

What are long-term consequences?

A
  • Cellulitis around bite withing 24 hours of infection
  • May develop into necrotizing fascitis or OSTEOMYELITIS
164
Q

What are the toxin mediated diseases caused by Staph Aureus?

Toxin responsible for each?

A
  • Scalded skin syndrome/impetigo: exfoliative toxin (protease)
  • Toxic shock syndrome: TSST a superantigen
  • Staph food poisoning: rapid onset w/ vomiting and associated with meats and mayonnaise left out too long
165
Q

How do differentiate Group A and Group B streptococcus using Bacitracin?

A
  • Group A = Bacitracin SENSITIVE
  • Group B = Bacitracin RESISTANT
166
Q

Which tests allows for us to distinguish Streptococcus Agalactiae (Group B) from all other strep?

A

cAMP test postive –> Group B plated with S. aureus it has a increasing zone of hemolysis

167
Q

What morphology will some RBCs have in Shigella infection?

A

Aggregates of platelets protruding from endothelium, lyse RBCs as they pass by, cutting some in half —> Shistocytes! (look like helmets)

168
Q

Primary cause of meningitis in infants from 3-36 months?

A

Influenza type b

169
Q

What does a false positive PPD skin test indicate?

A

Some people from other countries may have had BCG vaccine

170
Q

What is Pott’s disease?

A

Tuberculosis infection affecting the vertebrae, usually in thoracic and lumbar spine —> destroying IV discs and then adjacent vertebral bodies

171
Q

What is Tertiary Syphilis?

How long does it take to develop and what are the 3 general categories of pathologic finidings?

A
  • Develops over 6-40 years, w/ slow inflammatory damage to organ tissue, small BVs, and nerve tissue: grouped into 3 general categories.
    1) Gummatous: occurs 3-10 yrs after 1° = localized granulomatous lesions, which necrose and become fibrotic
    2) CV syphilis: occurs at least 10 yrs after 1° = aneurysm in ascending aorta or aortic arch; chronic inflammatory destruction of vasa vasorum
    3) Neurosyphilis: subacute meningitis, meningovascular syphills (cerebrovascular occlusion), Tabes dorsalis (damage to posterior columns and dorsal roots) leading to odd gait, general paresis, and the Argyll-Roberston pupil = accomodating, but non-reactive.
172
Q

Describe the life cycle of Chlamydia and its 2 forms.

A
  • Elementary body: metabollically inert (does not divide), infectious particle, attaches to and enters (via endocytosis) columnar epithelial cells that line mucous membranes
  • Reticulate body (initial body): once inside host cell, inhibits phagosome-lysosome fusion, grows in size and forms IB, can reproduce via binary fission and uses host ATP
  • Host cell liberates the EB, which can now infect more cells
173
Q

C. trachomatis can be passed to babies during delivery causing what infections?

What is the timeline for these symptoms and how can it be distinguished from gonorrhea?

How is diagnosis of each infection made?

A
  • Inclusion conjunctivitis: purulent yellow discharge and swelling of eyelids usually 5-14 days after birth
  • Dx made by demonstating basophilic intracytoplasmic inclusion bodies in cells taken from scrapings

- Infant pneumonia: usually occurs at 4-11 weeks of life; initally presenting w/ upper respiratory sx’s followed by rapid breathing, cough, and respiratory distress (gonorrhea presents 2-3 days after birth)

174
Q

What is special about the Rickettsial disease caused by Coxiella burnetii?

A

Only ricketssial disease that causes pneumonia and in which there is NO rash!

175
Q

What is the HACEK group of bacteria that are known to cause endocarditis?

A

Haemophilus species

Actinobacillus species

Cardiobacterium species

Eikenella species

Kingella species

176
Q

Which organism is the #1 cause of bacterial bronchitis and pneumonia in teenagers and young adults?

A

Mycoplasma pneumoniae

177
Q

What kind of infection is caused by Rickettsia typhi?

Reservoir and is transmitted how?

A
  • Causes endemic flea-borne typhus: fever, headache, and a flat and sometimes bumpy (maculopapular) rash. Milder sx’s than epidemic typhus (caused by Rickettisia prowazekii)
  • Reservoir = rodents
  • Transmission = rat flea (Xenopsylla cheopi)
178
Q

What are the 4 D’s of Botulism?

A
  1. Diplopia (double vision)
  2. Dysarthria (difficulty talking)
  3. Dysphonia (abnormal voice quality, pitch or intensity)
  4. Dysphagia (trouble swallowing)
179
Q

What is the JONES criteria for Rheumatic Fever?

A

J = joints (polyarthritis)

O = Myocarditis and pericarditis

N = nodules on extensor surfaces

E = Erythema marginatum

S = Sydenham’s Chorea

180
Q

What is caused by Klebsiella granulomatis?

Where is this infection endemic?

What are the signs and symptoms?

A
  • Granuloma inguinale
  • Endemic in rural areas of some developing countries
  • Begins as a raised papular lesion of the genitalia
  • Eventually ulcerates and develops abundant granulation tissue, mainfesting as a painless, beefy red ucler that bleeds readily on contact
181
Q

What is caused by Haemophilus ducreyi?

Where is it most commonly seen?

A
  • Chancroid = Painful genital ulcer with exudate, inguinal adenopathy

“It’s so painful, you “do cry”

  • Most common in tropical and subtropical areas among lower SE groups. One of the most common causes of genital ulcers in Africa and SE Asia
182
Q

Morphology of actinomyces israelii

A

Gram+ filamentous branching rod

Obligate anaerobe

183
Q

Clinical manifestations of actinomyces israelii infection?

Part of which normal flora?

What is the catalyst for infection?

A

Part of normal flora of oral cavity

Jaw trauma (such as with dental work) causes infection.

Starts as a lump and proceeds to form abscess.

Can then infect sinus tracts and drainage of yellow sulfur granule material

184
Q

Morphology of Nocardia asteroides

A

Gram+ filamentous branching rod

Weakly acid-fast d/t mycolic acids

Obligate aerobe

Catalase+

Urease+

Found in soil but does NOT form spores

185
Q

Clinical manifestations of Nocardia asteroides; who is primarily affected?

What are the 3 main infection sites

A

Primarily affects immunocompromised —> HIV pts, transplant pts, pts on glucocorticoids

Affects men > women

3 main sites of infection:

  • Pulmonary: PNA with lung abscesses (cavitary lesions)
  • CNS: brain abscesses
  • Cutaneous: pyogenic, indurated lesions (at risk when dirt gets in wounds)
186
Q

Why is it clinically significant to note if organisms are catalase+?

A

People with chronic granulomatous disease (CGD) are at increased risk of infection with catalase+ organisms

187
Q

A 52 yo patient with diabetic neuropathy is admitted to the MICU. He begins spiking a fever the day before while a patient in the dialysis unit. He is now hypotensive. You diagnose a urinary tract infection due to a urea-splitting agent.

Which bacteria is most likely in this setting?

A

Proteus mirabilis

188
Q

What are the characteristics of Acinetobacter baumannii**?

Where are they most often seen and what kind of infections do they cause?

Why are they so unique in the healthcare setting?

A
  • Aerobic, gram-negative
  • Can survive for extended periods on enviornmental surfaces, increasing its transmission in healthcare settings
  • Pneumonia, Line-related bacteremia, UTI, burn/wound infections, eye infections
  • At times may appear gram-positive and may even be misidentified as Neisseria species
189
Q

Which bacteria is an obligate aerobe, gram-negative rod and produces a green fluorescent pigment (pyoverdin) and blue pigment (pyocyanin), which gives colonies and infected wound dressings a greenish-blue coloration?

A

Pseudomonas aeruginosa

PCM II Final (10 decks)

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