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Board Review > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Gardnerella vaginalis - cell wall, Gram stain

A

A pleomorphic, gram-variable rod involved in

bacterial vaginosis

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2
Q

Gardnerella vaginalis - signs, and symptoms

A

Presents as a gray vaginal
discharge with a fishy smell; nonpainful (vs.
vaginitis). Associated with sexual activity, but
not sexually transmitted. Bacterial vaginosis
is also characterized by overgrowth of
certain anaerobic bacteria in vagina. Clue
cells, or vaginal epithelial cells covered with
Gardnerella bacteria (“stippled” appearance
along outer margins), are visible under the
microscope

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3
Q

Gardnerella vaginalis - treatment

A

metronidazole or clindamycin

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4
Q

Legionella pneumophilla - shape, Gram stain, culture

A

Gram-negative rod. Gram stains poorly—use
silver stain. Grow on charcoal yeast extract
culture with iron and cysteine.

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5
Q

Legionella pneumophilla - labs

A

Detected by
presence of antigen in urine. Labs may show
hyponatremia

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6
Q

Legionella pneumophilla - transmission

A

Aerosol transmission from
environmental water source habitat (e.g., air
conditioning systems, hot water tanks). No
person-to-person transmission

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7
Q

Legionella pneumophilla - treatment

A

macrolide or quinolone.

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8
Q

legionnaires disease versus Pontiac disease

A

Legionnaires’ disease—severe pneumonia
(often unilateral and lobar A ), fever, GI and
CNS symptoms.
Pontiac fever—mild flu-like syndrome.

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9
Q

Klebsiella - Gram stain, culture, capsule, urease, lactose,

A

gram-negative rod, MacConkey plates,
Very mucoid colonies caused by abundant
polysaccharide capsules
urease positive, fast lactose fermenter

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10
Q

Klebsiella – disease, signs

A

An intestinal flora that causes lobar pneumonia
in alcoholics and diabetics when aspirated.
Dark red “currant
jelly” sputum (blood/mucus).
Also cause of nosocomial UTIs.

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11
Q

helicobacter pylori - disease, complications of disease

A

Causes gastritis and peptic ulcers (especially duodenal). Risk factor for peptic ulcer, gastric
adenocarcinoma, and MALT lymphoma

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12
Q

helicobacter pylori - Gram stain, catalase, oxidase, urease, test for antigens and antibodies.

A

Curved gram-negative rod A that is catalase, oxidase,
and urease ⊕ (can use urea breath test or fecal antigen test for diagnosis). Creates alkaline
environment. serum IgG antibodies

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13
Q

helicobacter pylori - treatment

A

triple therapy: proton pump inhibitor + clarithromycin +

amoxicillin (or metronidazole if penicillin allergy)

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14
Q

Haemophilus influenzae - Gram stain, capsule, culture, quelling

A

Small gram-negative (coccobacillary) rod. capsule positive, Culture on chocolate agar, which
contains factors V (NAD+) and X (hematin)
for growth; can also be grown with S. aureus,
which provides factor V through the hemolysis
of RBCs. positive quelling reaction

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15
Q

Haemophilus influenzae - disease

A

Nontypeable strains are
the most common cause of mucosal infections
(otitis media, conjunctivitis, bronchitis) as well
as invasive infections since the vaccine for
capsular type b was introduced.

HaEMOPhilus causes Epiglottitis
A B (“cherry red” in children), Meningitis,
Otitis media, and Pneumonia.

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16
Q

Haemophilus influenza – vaccine, Virulence factors

A

Vaccine contains type b capsular polysaccharide
(polyribosylribitol phosphate) conjugated
to diphtheria toxoid or other protein. Given
between 2 and 18 months of age.

Produces IgA protease and PRP Capsule

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17
Q

Haemophilus influenza – treatment

A

Treat mucosal infections with amoxicillin
+/− clavulanate.
Treat meningitis with ceftriaxone. Rifampin
prophylaxis for close contacts.

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18
Q

Haemophilus ducreyi - clinical presentation

A

Chancroid - Painful genital ulcer with exudate, inguinal

adenopathy, presence of buboes

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19
Q

Francsiella tularensis - inside or outside the cell, anaerobic or aerobic, Gram stain,

A

facultative intracellular pathogen, anaerobic, gram-negative coccobacilli

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20
Q

Francsiella tularensis - disease and transmission factors.

A

tularemia - causing lymphadenopathy and fever. transmitted by ticks bite and deer fly, associated with rabbit skinning

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21
Q

Enterococci - Lancefield group, Gram stain, species

A

gram-positive cocci, group D strep, (E. faecalis and E. faecium)

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22
Q

Enterococci - laboratory test, salt, bile, hemolysis

A

Enterococci, hardier than nonenterococcal
group D, can grow in 6.5% NaCl and bile (lab
test). Variable hemolysis.

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23
Q

enterococci - disease, antibiotic resistance, sensitivities

A

normal colonic flora that are penicillin
G resistant and cause UTI, biliary tract
infections, and subacute endocarditis
(following GI/GU procedures). increasing resistance to vancomycin V (VRE), sensitive to ampicillin/amoxicillin and cephalosporins,

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24
Q

EHEC - Gram stain, number of identification

A

gram-negative rod
Also called STEC (Shiga toxin–producing
E. coli). O157:H7 is most common serotype in
U.S.

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25
Q

EHEC – toxin characteristics

A

Shiga-like toxin causes hemolytic-uremic

syndrome, attacks the 60 S ribosome, and increases cytokine release.

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26
Q

EHEC - disease in the bowels, bloodstream/kidneys. blood smear.

A

dysentery, as a toxin can cause necrosis and bowel inflammation
Shiga-like toxin causes hemolytic-uremic
syndrome: triad of anemia, thrombocytopenia,
and acute renal failure due to microthrombi
forming on damaged endothelium
Ž mechanical hemolysis (with schistocytes on
peripheral blood smear), platelet consumption,
and  renal blood flow.

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27
Q

EHEC - difference between E. coli strains in testing

A

Does not ferment sorbitol (distinguishes EHEC

from other E. coli).

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28
Q

E.coli - Gram stain, culture plates, test ( fermentation)

A

gram-negative rods, culture on Eosin-methylene blue plates leading to purple colonies with green sheen, pink colonies macConkey plates. lactose fermenter, catalase positive.

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29
Q

E. coli – virulence factors and disease

A

normal gut flora, some strains are pathogenic, often associated with diarrhea
Lipid A associated with bacterial sepsis, P Pili associated with UTI symptoms. K capsule associated with pneumonia and meningitis especially in infants.

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30
Q

Coxiella burnetii - Gram stain, inside the cell or outside the cell. preferred method of transmission (especially compared to other rickettsial diseases).

A

gram-negative, obligate intracellular bacteria, no arthropod vector. Spores inhaled as aerosols from cattle/sheep amniotic
fluid.

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31
Q

Coxiella burnetii - disease, what is missing compared to other rickettsial diseases? vascular manifestations.

A

presents with a fever and flulike symptoms, does not have a rash compared to other rickettsial diseases. Most common
cause of culture ⊝ endocarditis.

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32
Q

Corynebacterium diphtheriae - Gram stain, culture plate

A

gram-positive rods, black colonies on cystine-tellurite agar.

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33
Q

Corynebacterium diphtheriae - nature of toxin, encoded by?

A

exotoxin encoded by β-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.

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34
Q

Corynebacterium diphtheriae - laboratory findings (Aniline and methylene blue), vaccine.

A

Lab diagnosis based on gram-positive rods with
metachromatic (blue and red) granules and
⊕ Elek test for toxin.

Toxoid vaccine prevents diphtheria.

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35
Q

Clostridium tetani - Gram stain, aerobic or anaerobic

A

gram-positive, spore forming, obligate anaerobic.

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36
Q

Clostridium tetani - nature of toxin, effect on neurotransmitters, cell targets.

A

exotoxin - Produces tetanospasmin, an exotoxin causing
tetanus. Tetanus toxin (and botulinum toxin)
are proteases that cleave SNARE proteins for
neurotransmitters. Blocks release of inhibitory
neurotransmitters, GABA and glycine, from
Renshaw cells in spinal cord

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37
Q

Clostridium tetani – disease, treatment

A

Causes spastic paralysis, trismus (lockjaw), risus
sardonicus (raised eyebrows and open grin), opisthotonus (forced extension of the body)

prevent with a vaccine, treat with antitoxin and booster, diazepam for muscle spasms.

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38
Q

Clostridium perfringens – Gram stain, aerobic or anaerobic

A

gram-positive, spore forming, obligate anaerobic

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39
Q

Clostridium perfringens – G.I. disease and musculoskeletal disease, toxins

A

Produces α toxin (lecithinase, a phospholipase)
that can cause myonecrosis (gas gangrene A )
and hemolysis. food poisoning - from reheated meats, toxin based

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40
Q

Clostridium perfringens – treatment

A

hyperbaric oxygen slows bacterial growth, clindamycin

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41
Q

Clostridium difficile – Gram stain, anaerobic or aerobic

A

gram-positive rods, obligate anaerobic

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42
Q

Clostridium difficile – toxin production X 2, disease and aggravating factor

A

Produces 2 toxins. Toxin A, enterotoxin, binds
to the brush border of the gut. Toxin B,
cytotoxin, causes cytoskeletal disruption via
actin depolymerization Ž pseudomembranous
colitis B Ž diarrhea.

secondary to antibiotic use, usually clindamycin or ampicillin

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43
Q

C. difficile – diagnostics and treatment (antibiotics or otherwise

A

Diagnosed by detection one or both toxins in stool by PCR.

metronidazole or oral vancomycin. For recurrent cases, consider repeating prior regimen, fidaxomicin, or fecal microbiota transplant.

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44
Q

Clostridium botulinum – Gram stain, anaerobic or aerobic

A

gram-positive rod, obligate anaerobic

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45
Q

Clostridium botulinum – toxin, disease, transmission

A

Produces a preformed, heat-labile toxin that
inhibits ACh release at the neuromuscular
junction, causing botulism.

disease is caused by ingestion of preformed toxin. In
babies, ingestion of spores in honey causes
disease (floppy baby syndrome).

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46
Q

Clostridium botulinum – treatment

A

antitoxin

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47
Q

Chlamydia Trachomatis A through C - disease characteristics

A

Chronic infection, cause blindness due to

follicular conjunctivitis in Africa.

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48
Q

Chlamydia D through K – disease characteristics in women and in neonates

A

Urethritis/PID, ectopic pregnancy, neonatal
pneumonia (staccato cough) with eosinophilia,
neonatal conjunctivitis.

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49
Q

Chlamydia L1, L2, and L3 - disease characteristics and treatment.

A

Lymphogranuloma venereum—small, painless
ulcers on genitals Ž swollen, painful inguinal
lymph nodes that ulcerate (buboes). Treat with
doxycycline.

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50
Q

Chlamydia – staining, energy source, inside or outside the cell.

A

Chlamydia lacks muramic acid, making Gram stain impossible, stained with Giesma staining instead, obligate intracellular pathogen.

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51
Q

Chlamydia – lifecycle

A

Elementary body (small, dense)
is “Enfectious” and Enters cell via
Endocytosis; transforms into reticulate body.
Reticulate body Replicates in cell by fission;
Reorganizes into elementary bodies.

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52
Q

Chlamydia – disease, joints, eyes, urogenital, lungs.

A

Chlamydia trachomatis causes reactive arthritis
(Reiter syndrome), follicular conjunctivitis A ,
nongonococcal urethritis, and PID.

C. pneumoniae and C. psittaci cause atypical
pneumonia; transmitted by aerosol.

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53
Q

Chlamydia – laboratory test

A

Lab diagnosis: cytoplasmic inclusions seen on

Giemsa or fluorescent antibody–stained smear.

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54
Q

Campylobacter jejuni - Gram stain, shape, oxidase, growth characteristics

A

gram-negative rod, corkscrew shape, with flagella, oxidase positive, grows well at 42°C

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55
Q

Campylobacter – primary disease, potential complications of disease

A

major cause of bloody diarrhea especially in children, can potentially lead to Guillain-Barré syndrome and
reactive arthritis.

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56
Q

Campylobacter – mode of transmission

A

Fecal-oral transmission through person to-
person contact or via ingestion of poultry, meat, unpasteurized milk. Contact with infected
animals (dogs, cats, pigs) is also a risk factor. puppies with diarrhea.

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57
Q

Brucella – Gram stain, inside or outside the cell

A

gram-negative coccobacilli, facultative intracellular bacteria

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58
Q

Brucella – primary disease, mode of transmission

A

Brucellosis/undulant fever, unpasteurized milk

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59
Q

Borrelia burgdorferi – bacterial class, visualization

A

spirochete, do not Gram stain well, dark field microscopy or Giesma stain. silver stain works as well

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60
Q

Borrelia burgdorferi – disease vector, primary location

A

the Ixodes tick, field mouse which is the primary disease vector, most common in the northeastern part of the United States.

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61
Q

Borrelia burgdorferi - early and late symptoms, connective tissue and neurological

A

Initial symptoms—erythema chronicum
migrans B , flu-like symptoms, +/− facial
nerve palsy.

Later symptoms—monoarthritis (large
joints) and migratory polyarthritis, cardiac
(AV nodal block), neurologic (meningitis,
facial nerve palsy, polyneuropathy).

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62
Q

Borrelia burgdorferi - treatment

A

doxycycline, ceftriaxone.

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63
Q

Bartonella pertussis – Gram stain, culture plate x2

A

gram-negative Coccoid, Bordet-Gengou Agar (potato), Regan-Lowe medium (Charcoal, blood, and antibiotic)

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64
Q

Bordetella pertussis - treatment

A

macrolides, most likely erythromycin or azithromycin

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65
Q

Bordetella pertussis - toxin, changes to blood differentials

A

Pertussis toxin AB ADP ribosylating toxin
Overactivates adenylate cyclase ( cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe, causes lymphocytosis and hyperinsulinemia.

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66
Q

Bordetella pertussis - disease

A

Whooping cough—child coughs on expiration
and “whoops” on inspiration (toxin may
not actually be a cause of cough; can cause
“100-day cough” in adults)

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67
Q

Bartonella henselae - Gram stain

A

gram-negative rod

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68
Q

Bartonella henselae - primary diseases

A

cat scratch fever, which presents as profuse lymphadenopathy and lymphangitis, bacillary angiomatosis, which presents as neoplastic growths of vessels on the skin and on visceral organs secondary to Bartonella infection.

Infection is rare within the immunocompromised, and can frequently show up in AIDS patients. Can be confused with Kaposi’s sarcoma.

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69
Q

Bartonella henselae - findings on pathology

A

granuloma formation

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70
Q

Bacteroides Fragilis - staining, anaerobes or aerobes, typical location.

A

gram-negative Rod, anaerobic, part of the natural colonic flora, makes vitamin K.

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71
Q

Bacteroides Fragilis - disease, G.I. and lung

A

can lead to abdominal abscess formation, associated with aspiration pneumonia and can lead to lung abscess

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72
Q

Bacteroides Fragilis - treatment, resistance, and sensitivities

A

resistant to beta-lactam antibiotics, sensitive to clindamycin and metronidazole.

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73
Q

Bacillus Cereus - Gram stain, aerobic or anaerobic, red cells on agar plates?

A

gram-positive rods with spores, anaerobic, beta hemolytic

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74
Q

Bacillus Cereus - disease, two types, type of toxin

A

Causes food poisoning. Spores survive cooking
rice. Keeping rice warm results in germination
of spores and enterotoxin formation.

Emetic type usually seen with rice and pasta.
Nausea and vomiting within 1–5 hr. Caused
by cereulide, a preformed toxin.

Diarrheal type causes watery, nonbloody
diarrhea and GI pain within 8–18 hr.

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75
Q

Bacillus anthracis - Gram stain, special nature of the cell wall

A 
gram-positive rods with spores, only bacteria to have
polypeptide capsule (contains d-glutamate).
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76
Q

Bacillus anthracis - nature of disease on skin

A

Painless papule surrounded by vesicles, ulcer
with black eschar ( A , right) (painless,
necrotic) uncommonly progresses to
bacteremia and death.

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77
Q

Bacillus anthracis - pulmonary disease, variant associated with specific animal

A

Inhalation of spores flu-like symptoms
that rapidly progress to fever, pulmonary
hemorrhage, mediastinitis, and shock

Woolsorters disease - pulmonary variant of anthrax developed from inhalation from spores produced in sheep’s wool.

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78
Q

Bacillus anthracis - toxin formation

A

edema toxin - increases cyclic AMP levels within the cell, Likely responsible for characteristic edematous
borders of black eschar in cutaneous anthrax.

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79
Q

Actinomyces - Gram stain

A

Gram-positive anaerobe, long branching filaments

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80
Q

Actinomyces - normal location, disease, distinguishing characteristics, treatment

A

part of the normal mouth flora, disease can be provoked by dental trauma. Bacterial sinus tracts with pus. Also associated with IUDs and cervititis

sulfur granule formation

treatment with penicillin

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81
Q

Neisseria Gonoccocci - gram stain and Culture agar x 2, relationship with neutrophils

A

Gram Negative diploccocci and grow Thayer Martin or Chocolate Agar, fastitious organism, often inside neutrophils.

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82
Q

Neisseria Gonoccocci - Disease? Women and in children? joints?

A

Causes gonorrhea, septic arthritis, neonatal
conjunctivitis, pelvic inflammatory disease
(PID), and Fitz-Hugh–Curtis syndrome

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83
Q

Neisseria Gonoccocci - Treatment and prevention, adults and neonates.

A

Condoms decrease sexual transmission. Erythromycin
ointment prevents neonatal transmission. Treat with ceftriaxone + (azithromycin
or doxycycline) for possible chlamydial
coinfection

84
Q

Neisseria Gonoccocci - Capsule?, Maltose and glucose Fermentation? Vaccine?

A

No polysaccharide capsule, No maltose fermentation, No vaccine due to antigenic variation of pilus
proteins,

85
Q

Mycoplasma Pneumoniae - gram stain and culture, cell membrane component

A

no cell wall leads to no gram stain. Culture in Eaton’s Agar with mulberry colonies (pleomorphic). Bacterial membrane contains sterols for stability.

86
Q

Mycoplasma Pneumoniae - disease presentation, symptoms.

A

Classic cause of atypical “walking” pneumonia
(insidious onset, headache, nonproductive
cough, patchy or diffuse interstitial infiltrate).

87
Q

Mycoplasma Pneumoniae - affected population

A

Mycoplasmal pneumonia is more common in

patients

88
Q

Mycoplasma Pneumoniae - findings on X-ray, Antibodies production, Treatment

A 
X-ray looks worse than patient. High titer of
cold agglutinins (IgM) which can lead to hemolytic anemia.

macrolides, doxycycline, or
fluoroquinolone (penicillin ineffective since
Mycoplasma have no cell wall).

89
Q

TB - primary infection, Parynchemal findings and lymphatic changes. Progression? HIV?

A

Ghon focus (usually in lower to mid zones of lung), this plus hilar lymphadenopathy on xray = Ghon complex.

Heals by Fibrosis -> Immunity and hypersensitivity ->
Tuberculin

If you have HIV -> Progressive lung disease (HIV, malnutrition) -> Death (rare)

90
Q

TB - Primary infection -> Bacteremia?

A

Miliary tuberculosis -> Death

91
Q

TB - Primary Infection -> Preallergic lymphatic or

hematogenous dissemination -> ?

A

Dormant tubercle bacilli in several organs -> Reactivation in Adult Life.

92
Q

TB - Secondary Infection -> Presentation

A

Fibrocaseous cavitary lesion(usually upper lobes) -> Reactivation tuberculosis of the lungs

93
Q

TB - Extrapulmonary Dz

A
  • CNS (parenchymal tuberculoma or meningitis)
  • Vertebral body (Pott disease)
  • Lymphadenitis • Renal • GI • Adrenals
94
Q

Reading a postive PPD, IGRA?

A

PPD ⊕ if current infection or past exposure.
False positives with BCG vaccination (further
workup required).

Interferon-γ release assay (IGRA) has fewer false
positives from BCG vaccination

95
Q

Reading a Negtive PPD

A

PPD ⊝ if no infection or anergic (steroids,
malnutrition, immunocompromise) and in
sarcoidosis.

96
Q

Mycobacteria - Cell wall, staining

A

Mycolic Acid in Cell wall, staining woth Carbofuschin lead to acid fast staining.

97
Q

TB - Symptoms, Respiratory?

A

TB symptoms include fever, night sweats,
weight loss, cough (nonproductive or
productive), hemoptysis.

98
Q

TB - Virulence Factors x 2

A

Cord factor in virulent strains inhibits
macrophage maturation and induces release of
TNF-α.

Sulfatides (surface glycolipids) inhibit
phagolysosomal fusion.

99
Q

M. scrofulaceum - Disease

A

(cervical lymphadenitis in

children).

100
Q

M. marinum - Disease

A

(hand infection in aquarium

handlers).

101
Q

M. avium – intracellulare, Disease and prophylaxis

A

disseminated, non-TB disease in AIDS; often resistant to

multiple drugs). Prophylaxis with azithromycin

102
Q

Mycobacterium leprae - gram stain, culture

A

acid-fast bacillus, can not be grow in vitro.

103
Q

Mycobacterium leprae - Disease Presentation, hand and feet

A

Likes cool temperatures (infects
skin and superficia nerves—“glove and
stocking” loss of sensation

104
Q

Mycobacterium leprae - More Benign presentation? T T- Helper Cells Response Treatment?

A

Tuberculoid—limited to a few hypoesthetic,
hairless skin plaques; characterized by high
cell-mediated immunity with a largely Th1-
type immune response

Treatment is dapsone and rifampin

105
Q

Mycobacterium leprae - most serious presentation? T- Helper Cells Response? Treatment?

A

Lepromatous—presents diffusely over the
skin, with leonine (lion-like) facies , and
is communicable; characterized by low cell mediated
immunity with a humoral Th2
response.

dapsone and rifampin + clofazmime

106
Q

Listeria monocytogenes - gram stain, inside or outside the cell. Oxidase. Hemolysis.

A

Gram Positive Coccobacilli, Facultative intracellular microbe Oxidase positive, Beta Hemolytic.

107
Q

Listeria monocytogenes - Transmission, adults and children.

A

unpasteurized dairy products
and cold deli meats, via transplacental
transmission, or by vaginal transmission
during birth

108
Q

Listeria monocytogenes - movement in the cell and outside the cell. Toxin?

A

Forms “rocket tails” A (via actin polymerization) that allow intracellular movement and cell-to-cell spread across cell membranes, thereby avoiding antibody.
Characteristic tumbling motility

Is only grampositive organism to produce endotoxin

109
Q

Listeria monocytogenes - Disease in Adults and Neonates. Pregnant women? Healthy people vs the immuno

A 
amnionitis, septicemia, and
spontaneous abortion in pregnant
women; granulomatosis infantiseptica;
neonatal meningitis; meningitis in
immunocompromised patients; mild
gastroenteritis in healthy individuals.
110
Q

Neisseria Meningitidis - Gram Stain, Capsule,Fermentation

A

Gram Negative Diplococci, Capsule Postive, Fermentation of Glucose and Maltose, Oxidase Positive,

111
Q

Neisseria Meningitidis - preventation, transmission, Treatment (prophylaxis)

A

Vaccine (type B vaccine not widely available

Transmitted via respiratory and oral secretions

Rifampin, ciprofloxacin, or ceftriaxone
prophylaxis in close contacts

Treatment: ceftriaxone or penicillin G

112
Q

Novobiocin - differences between Staphylococcus epidermidis and Staphylococcus Saprophyticus

A

NOvobiocin—Saprophyticus is Resistant;
Epidermidis is Sensitive.

On the office’s “staph” retreat, there was
NO StRESs.

113
Q

Optochin differences between strep. viridians and strep pneumoniae

A

Optochin—Viridans is Resistant; Pneumoniae is Sensitive.

OVRPS (overpass)

114
Q

Bacitracin differences between group and group B strep

A

group B is resistant group a is sensitive

B- BR AS

115
Q

definition of alpha hemolytic bacteria, organisms that fall into this class x 2

A

Form green ring around colonies on blood agar A . Include the following organisms:
ƒƒ Streptococcus pneumoniae (catalase ⊝ and optochin sensitive)
ƒƒ Viridans streptococci (catalase ⊝ and optochin resistant)

116
Q

beta hemolysis, definition and bacteria that fall into this group x 4

A

Form clear area of hemolysis on blood agar A . Include the following organisms:
ƒƒ Staphylococcus aureus (catalase and coagulase ⊕)
ƒƒ Streptococcus pyogenes—group A strep (catalase ⊝ and bacitracin sensitive)
ƒƒ Streptococcus agalactiae—group B strep (catalase ⊝ and bacitracin resistant)
ƒƒ Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk)

117
Q

Staphylococcus aureus – Gram stain, virulence factor, area of colonization

A

Gram-positive cocci in clusters A . Protein A (virulence factor) binds Fc-IgG, inhibiting complement activation and phagocytosis. Commonly colonizes the nares.

118
Q

common natures of infection, bone, skin, lung. - sTAPHYLOCOCCUS AUREUS

A

skin infections,
organ abscesses, pneumonia (often after
influenza virus infection), endocarditis,
septic arthritis, and osteomyelitis

119
Q

three types of toxins produced by staff aureus

A

Toxin-mediated disease—toxic shock
syndrome (TSST-1), scalded skin syndrome
(exfoliative toxin), rapid-onset food
poisoning (enterotoxins

120
Q

nature of Staphylococcus aureus toxic shock syndrome, presentation, common population x 2

A

Staphylococcal toxic shock
syndrome (TSS) presents as fever, vomiting,
rash, desquamation, shock, end-organ failure.
Associated with prolonged use of vaginal
tampons or nasal packing.

121
Q

Staphylococcus food poisoning, causative agent, timeframe, type of diarrhea produced. elimination by means of heat?

A

ingestion of preformed toxin. short incubation period
(2–6 hr) followed by nonbloody diarrhea
and emesis. Enterotoxin is heat stable Ž not
destroyed by cooking.

122
Q

implications of bacterial coagulase

A

Forms fibrin clot around self which can lead to abscess.

123
Q

Staphylococcus epidermidis , presence of coagulase, type of infection produced, meaning of presence in blood cultures. relationship with Novobiocin

A

Staphylococcus epidermidis - Infects prosthetic devices (e.g., hip implant, heart valve) and intravenous catheters by producing
adherent biofilms. Component of normal skin flora; contaminates blood cultures. Novobiocin
sensitive.

124
Q

Staphylococcus saprophyticus - most common site of infection relationship with novobiocin

A

Second most common cause of uncomplicated UTI in young women (first is E. coli). Novobiocin
resistant.

125
Q

streptococcus pneumoniae - most common cause of ( four diseases). relationship with OPtochin

A 
Most common cause of:
ƒƒMeningitis
ƒƒOtitis media (in children)
ƒƒ Pneumonia
ƒƒ Sinusitis

Optochin sensitive

126
Q

Streptococcus pneumoniae – Gram stain, virulence factors.

A

Lancet-shaped, gram-positive diplococci A . Encapsulated. IgA protease

127
Q

Streptococcus pneumoniae – type of sputum produced, relationship with sickle cell

A

Pneumococcus is associated with “rusty”
sputum, sepsis in sickle cell disease and
splenectomy

128
Q

Viridans group streptococci - Gram stain, hemolytic pattern, associated with what oral pathology?

A

α-hemolytic. They are normal flora of the oropharynx that cause dental caries (Streptococcus mutans).

129
Q

Viridans group streptococci - most commonly associated with what vascular pathology. what factor are made it allows this to happen?

relationship to optochin

A

subacute bacterial endocarditis at damaged heart
valves (S. sanguinis).

S. sanguinis
makes dextrans, which bind to fibrin-platelet
aggregates on damaged heart valves

optochin resistant

130
Q

group a Streptococcus, types of diseases caused: Pyogenic - face, nasopharynx, skin

A

Pharyngitis, cellulitis, impetigo, erysipelas

131
Q

group a Streptococcus - toxigenic diseases x 3

A

scarlet fever, toxic shock–like syndrome, necrotizing fasciitis

132
Q

group a Streptococcus immunogenic diseases X 2

A

rheumatic fever, glomerulonephritis

133
Q

group a Streptococcus - relationship with bacitracin, hemolytic pattern, PYR

effect of antibodies against M protein.

A

bacitracin sensitive, beta hemolytic, PYR positive.

antibodies against them protein can lead to autoimmune rheumatic fever.

134
Q

but titer is used to detect Strep Pyogenes

A

ASO titer,

135
Q

categories of the Jones criteria

A 
J♥NES (major criteria for acute rheumatic
fever):
Joints—polyarthritis
♥—carditis
Nodules (subcutaneous)
Erythema marginatum
Sydenham chorea
136
Q

scarlet fever - manifestations, skin, and mouth, causative agent

A

scarlet rash with sandpaper-like
texture, strawberry tongue, circumoral pallor,
subsequent desquamation.

Streptococcus pyogenes.

137
Q

Streptococcus agalactiae (group B streptococci), relationship with bacitracin, hemolytic pattern, Gram stain.

A

Bacitracin Resistant, beta hemolytic, gram-positive cocci in chains

138
Q

Streptococcus agalactiae (group B streptococci), typical area of colonization, diseases causing young children, lungs and brain

A

colonizes vagina; causes pneumonia, meningitis, and

sepsis, mainly in babies

139
Q

Streptococcus agalactiae (group B streptococci) - relationship with Staphylococcus aureus ( specific factor produced), H_______ test?

A

Produces CAMP factor, which enlarges the
area of hemolysis formed by S. aureus. (Note:
CAMP stands for the authors of the test, not
cyclic AMP.) Hippurate test ⊕

140
Q

Streptococcus agalactiae (group B streptococci) - procedures in dealing with pregnant women, what prophylaxis do they receive

A

Screen pregnant women at 35–37 weeks of
gestation. Patients with ⊕ culture receive
intrapartum penicillin prophylaxis

141
Q

Enterococci (group D

streptococci) - normal location, diseases caused, bowels, GU, vascular

A

normal colonic flora that are penicillin
G resistant and cause UTI, biliary tract
infections, and subacute endocarditis
(following GI/GU procedures)

142
Q

The definition of Lancesfield group

A

Lancefield grouping is based on differences in

the C carbohydrate on the bacterial cell wall.

143
Q

Enterococci (group D

streptococci), growth in bile, salt, hemolytic pathway

A

positive growth in bile, 6.5% sodium chloride, and has a variable hemolysis.

144
Q

Streptococcus bovis (group D streptococci), growth in bile, salt

A

does not grow in Bile or salt

145
Q

Streptococcus bovis - (specific species), potential vascular pathology. Association with what disease.

A

Colonizes the gut. S. gallolyticus (S. bovis
biotype 1) can cause bacteremia and subacute
endocarditis and is associated with colon
cancer.

146
Q

only way to eliminate spores

A

Must autoclave to
potentially kill spores (as is done to surgical
equipment) by steaming at 121°C for 15
minutes.

147
Q

spore producing bacteria

A 
Bacillus anthracis Anthrax
Bacillus cereus Food poisoning
Clostridium botulinum Botulism
Clostridium difficile Antibiotic-associated
colitis
Clostridium perfringens Gas gangrene
Clostridium tetani Tetanus
Coxiella burnetii Q fever
148
Q

Toxin responsible for the production of Emetic type of food poisoning caused by Bacillis Cereus

A

Spores survive cooking
rice. Keeping rice warm results in germination
of spores and enterotoxin formation

149
Q

Nocardia - Gram stain, aerobic or anaerobic, typical location.

A

gram-positive aerobic, typically found within the soil

150
Q

Nocardia - acid fast? Population of infection?, treatment?

A

Causes pulmonary infections in
immunocompromised and cutaneous infections
after trauma in immunocompetent.

treat with Sulfonimides (Bactrim)

151
Q

gram-negative bacteria that are oxidase positive and, shaped.

A

Campylobacter, Heliobacter, vibrio cholerae

152
Q

the only lactose non-fermenting, oxidase positive bacteria

A

Pseudomonas

153
Q

lactose fermenters ( shown by MacConkey Plate. How does E. coli break down lactose?

A 
Citrobacter, Klebsiella, E. coli, Enterobacter,
and Serratia (weak fermenter). E. coli produces
β-galactosidase, which breaks down lactose
into glucose and galactose.

Lactose is key.
Test with MacConKEE’S agar.

154
Q

gram-negative Coccoid or Coccibacilli bacteria

A 
Haemophilus influenzae
(requires factors V and X)
Pasteurella—animal bites
Brucella—brucellosis
Bordetella pertussis
155
Q

oxidase negative bacteria - TSI plate positive versus negative

A

Produces H2S on TSI Agar
Salmonella Proteus Yersinia

do not produce H2S on TSI
Shigella

156
Q

EMB agar— characteristics, used to distinguish what type of bacteria?

A

lactose fermenters grow as purple/
black colonies. E. coli grows colonies with a
green sheen.

157
Q

Pseudomonas aeruginosa - aerobic or anaerobic, Gram stain, oxidase positive or negative

A

Aerobic, motile, gram-negative rod. Non-lactose

fermenting, oxidase ⊕

158
Q

Pseudomonas aeruginosa - type of pigment produced, smell from culture, type of toxins produced,x 2 effects of said toxin

A

Produces pyocyanin
(blue-green pigment A ); has a grape-like odor.
Produces endotoxin (fever, shock) and exotoxin
A (inactivates EF-2).

159
Q

Pseudomonas - diseases and associations

A 
PSEUDDOmonas is associated with:
ƒƒ Pneumonia
ƒƒ Sepsis
ƒƒOtitis Externa (swimmer’s ear)
ƒƒUTIs
ƒƒDrug use
ƒƒDiabetes
ƒƒOsteomyelitis (e.g., puncture wounds).
160
Q

treatment for Pseudomonas: one of six antimicrobial classes.

A

ƒƒ Extended-spectrum β-lactams (e.g.,
piperacillin, ticarcillin, cefepime)
ƒƒ Carbapenems (e.g., imipenem, meropenem)
ƒƒMonobactams (e.g., aztreonam)
ƒƒ Fluoroquinolones (e.g., ciprofloxacin)
ƒƒ Aminoglycosides (e.g., gentamicin,
tobramycin)
ƒƒ For multidrug-resistant strains: colistin,
polymyxin B

161
Q

Ecthyma gangrenosum - causative agent, presentation, primary population

A

rapidly progressive,
necrotic cutaneous lesion B caused by
Pseudomonas bacteremia. Typically seen in
immunocompromised patients

162
Q

E. coli virulence factor - fibrimae and disease association

A

fimbriae—cystitis and pyelonephritis

163
Q

EIEC - disease, similarity to what other disease.

A

Microbe invades intestinal mucosa and

causes necrosis and inflammation, behave similarly to Shigella. needs to dysentery

164
Q

EPEC - disease, population affected

A

No toxin produced. Adheres to apical surface,
flattens villi, prevents absorption.
Diarrhea, usually in children

165
Q

hemolytic-uremic syndrome - causative toxin, clinical triad, signs on blood smear

A

Shiga like toxin, clinical triad of thrombocytopenia, anemia, and acute renal failure. due to microthrombi forming on damaged endothelium

mechanical hemolysis (with schistocytes on peripheral blood smear), platelet consumption, and  renal blood flow.

166
Q

EHEC - difference between other E. coli ( fermenting)

A

does not ferment sorbitol

167
Q

the four A’s of Klebsiella

A 
4 A’s of KlebsiellA:
Aspiration pneumonia
Abscess in lungs and liver
Alcoholics
di-A-betics
168
Q

Salmonella typhi – mode of dissemination, production of hydrogen sulfide? presence of flagella? primary reservoirs

A

Humans only, Can disseminate hematogenously, can produce hydrogen sulfide, has flagella

169
Q

Salmonella typhi – primary virulence factors x 2, infectious dose high or low, decision to give antibiotics

A

Vi capsule and the LPS, infectious dose is high ( inactivated by gastric acid), antibiotics prolonged duration of disease

170
Q

Salmonella typhi- primary immune cell, G.I. manifestations, vaccines x 2.

A

Primarily monocytes, constipation then followed by diarrhea, Oral

vaccine contains live attenuated S. typhi IM vaccine contains Vi
capsular polysaccharide.

171
Q

clinical manifestations of typhoid fever,, skin,, , G.I., constitutional. Treatment. relationship with the gallbladder

A

Causes typhoid fever (rose spots on abdomen,
constipation, abdominal pain, fever); treat with ceftriaxone or fluoroquinolone

can lead to chronic carrier state within the gallbladder

172
Q

Salmonella spp, - primary carriers of disease, production of hydrogen sulfide, means of dissemination.

A

Humans and animals, Can disseminate

hematogenously, can produce hydrogen sulfide

173
Q

Salmonella spp, - presence of flagella?, virulence factor, infectious dose high or low

A

it does have a flagella, only virulence factor is LPS, infectious dose is high.

174
Q

Salmonella spp, - effects of antibiotics on disease course, primary immune cells and disseminated disease, G.I. manifestations

A

Salmonella spp, - antibiotics Langton disease course, the primary immune cells and disseminated disease is neutrophils, G.I. manifestations include bloody diarrhea.

175
Q

Salmonella spp, - vaccine?

A

no vaccine

176
Q

Salmonella spp, - primary source of infections, relationship with gastroenteritis

A

Poultry, eggs, pets, and turtles are common sources. Gastroenteritis is
usually caused by nontyphoidal Salmonella.

177
Q

Shigella – primary carrier, means of dissemination, presence of flagella, production of hydrogen sulfide?

A

primary carriers humans, bacteria leads cell to cell no hematogenous spread, no presence of flagella, cannot produce hydrogen sulfide.

178
Q

Shigella – virulence factors X 2, infectious does high or low. use of antibiotics and chains and duration of infection.

A

Shiga toxin and LPS. infectious doses low because it is resistant to gastric acid. antibiotics shorten duration.

179
Q

Shigella - primary cells in immune response, G.I. manifestations, presence of vaccine.

A

PMNs are the primary immune cells , bloody diarrhea, no vaccine for Shigella. Invasion is the key to pathogenicity; organisms that produce little toxin can cause disease due to invasion.

180
Q

what are the four F’s of Shigella transmission

A

Four F’s: Fingers, Flies, Food, Feces

181
Q

Shigella – species x 4 (decreasing order of severity)

A

In order of decreasing severity (less toxin produced): S. dysenteriae, S. flexneri, S. boydii, S. sonnei

182
Q

Shigella – what is the primary key of pathogenicity

A

Invasion is the key to pathogenicity;
organisms that produce little toxin
can cause disease due to invasion

183
Q

Vibrio cholerae - disease manifestations, nature of cholera toxin, oxidase?

A

Produces profuse rice-water diarrhea via enterotoxin that permanently activates Gs,  cAMP, Comma shaped , oxidase ⊕,

184
Q

vibrio cholerae - relationship with pH, necessary palliative therapy

A

grows in alkaline media. Endemic to developing countries.

Prompt oral rehydration is necessary.

185
Q

Yersinia enterocolitica - primary mode of transmission ( animals and food), disease manifestation (GI)

A

Usually transmitted from pet feces (e.g., puppies), contaminated milk, or pork. Causes acute
diarrhea or pseudoappendicitis (right lower abdominal pain due to mesenteric adenitis and/or
terminal ileitis).

186
Q

Spirochetes - members, shape, visualization ( dyes, microscopy)

A

Spiral-shaped bacteria with axial filaments. Includes Borrelia (big size), Leptospira, and Treponema

Only Borrelia can be visualized using aniline dyes (Wright or Giemsa stain) in light microscopy A due to size. Treponema is
visualized by dark-field microscopy.

187
Q

Leptospira interrogans - primary disease, primary vector, disease presentation ( constitutional, skin, eyes).

A

Found in water contaminated with animal urine, causes leptospirosis—flu-like symptoms,
myalgias (classically of calves), jaundice, photophobia with conjunctival suffusion (erythema
without exudate).

188
Q

leptospirosis - population of infection and location

A

Prevalent among surfers and in tropics (i.e., Hawaii).

189
Q

icterohemorrhagic leptospirosis)— also known as…? Causes dysfunction in what two organs? disease manifestations

A

Weil disease, severe form with jaundice and azotemia from liver
and kidney dysfunction, can also lead to fever, anemia, hemorrhage.

190
Q

primary syphilis - disease manifestation, visualization of bacteria. Other test

A

Localized disease presenting with painless chancre. If available, use dark-field microscopy to visualize treponemes in fluid from chancre . VDRL ⊕ in ~ 80%

191
Q

secondary syphilis - symptoms, constitutional, skin, genitals. Confirmatory microscopy.

A

Disseminated disease with constitutional symptoms, maculopapular rash (including palms and soles, condylomata lata (smooth, moist, painless, wart-like white lesions on genitals); also confirmable with dark-field microscopy.

192
Q

tertiary syphilis - symptoms, skin, vascular, eyes, neurological.

A

Gummas (chronic granulomas), aortitis (vasa vasorum destruction), neurosyphilis (tabes dorsalis,
“general paresis”), Argyll Robertson pupil (constricts with accommodation but is not reactive to
light; also called “prostitute’s pupil” since it accommodates but does not react).

193
Q

tertiary syphilis – signs, laboratory test for neurosyphilis

A

broad-based ataxia, ⊕ Romberg, Charcot joint ( primarily in the knee and hip), stroke without hypertension.
For neurosyphilis: test spinal fluid with VDRL and PCR.

194
Q

secondary syphilis- laboratory test, results during latent phase

A

Serologic testing: VDRL/RPR (nonspecific), confirm diagnosis with specific test (e.g., FTA-ABS).
Secondary syphilis = Systemic. Latent syphilis (⊕ serology without symptoms) follows.

195
Q

VDRL - reagents used in the test, specificity?, noted false positives

A

VDRL detects nonspecific antibody that reacts
with beef cardiolipin. Inexpensive, widely
available test for syphilis, quantitative, sensitive but not specific.

Viral infection (mono, hepatitis)
Drugs
Rheumatic fever
Lupus and leprosy

196
Q 
Jarisch-Herxheimer
reaction - symptoms, causative agent, class of bacteria usually involved
A

Flu-like syndrome (fever, chills, headache, myalgia) after antibiotics are started; due to killed
bacteria (usually spirochetes) releasing endotoxins.

197
Q

Anaplasma - disease, vector, signs on microscopy.

A

Anaplasmosis Ixodes ticks (live on deer and mice), Granulocytes with
morulae in cytoplasm

198
Q

Borrelia recurrentis - disease, vector

A

relapsing fever, Louse (recurrent due to variable surface

antigens)

199
Q

Pasteurella multocida - disease, vector

A

cellulitis and osteomyelitis, spread thru dog and cat bites

200
Q

Yersinia pestis, disease, vector

A

Plague, Fleas (rats and prairie dogs are reservoir)

201
Q

treatment for all rickettsial diseases

A

doxycycline

202
Q

Rickettsia rickettsii - disease, primary vector, and primary location. primary disease triad

A

Rickettsia rickettsii, vector is tick. Despite its
name, disease occurs primarily in the South
Atlantic states, especially North Carolina.

Classic triad—headache, fever, rash (vasculitis).

203
Q

Rickettsia rickettsii - location of the rash, ending location of rash

A

Rash typically starts at wrists and ankles and
then spreads to trunk, palms, and Palms and soles rash is seen in

Coxsackievirus
A infection (hand, foot, and mouth disease),
Rocky Mountain spotted fever, and 2° Syphilis
(you drive CARS using your palms and soles).soles

204
Q

R. typhi - disease, primary disease vector

A

endemic typhus, spread by fleas

205
Q

R. prowazekii - disease, primary vector

A

epidemic typhus, human body louse

206
Q

typhus - rash?

A

Rash starts centrally and spreads out, sparing

palms and soles.

207
Q

Candida . ____________and___________ at 20°C

. ____________ at 37°C

A

Pseudohyphae; budding yeasts; germ tubes

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