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Clinical Microbiology Lecture > Exam 2 > Flashcards

Exam 2 Flashcards

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Biology 101 flashcards
0
Q

Listeria monocytogenes Characteristics

A 
G+B
Non-branching
Short chains, pairs
CAT+
CAMP+
Weak beta hemolysis 
Facultative, high NaCl
Tumbling motility
Wide temp and pH range
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1
Q

Listeria spp.

A

G+B
Aerobes
Non spore-forming

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2
Q

Listeria monocytogenes pathogenesis

A

Contact via contaminated food/water
Intercellular pathogen - avoid clearance by humoral immunity - T cell defect patients highly susceptible
Bacterial endotoxin: listeriolysin O (activated by phagolysosome acidity)
Moves cell to cell via filipod

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3
Q

Listeria monocytogenes clinical disease

A

Neonate: early onset - in utero - abortion, stillbirth, premie
Late onset - 2-3 weeks - meningitis or meningoencephalitis with septicemia

Adult: asymptomatic, flu-like, meningitis, bacteremia

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4
Q

Erysipelothrix rhusiopathiae characteristics

A 
G+B
Non-spore forming
Microaerophilic or high CO2 
CAT- 
Non-motile
H2S+
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5
Q

Erysipelothrix rhusiopathiae pathogenesis

A

Neuramidase: attachment and penetration into epithelial cells

Capsule

Found on swine and turkeys, zoonotic infection - occupational risk: meat processors, pig farmers, poultry workers, fish handlers and vets

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6
Q

Erysipelothrix rhusiopathiae clinical disease

A

Erysipeloid - localized skin infection, violet, pruritic (itchy) rash on fingers and hands

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7
Q

Corynebacterium spp characteristics

A 
G+B 
Aerobic 
"Coryneform" club shaped bacilli 
CAT+
Non-motile
Fermenters 
Metachromatic granules with special stains
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8
Q

Corynebacterium spp. Pathogenesis

A

Found in plants, animals, and colonize human skin, upper respiratory tract, GI and urogenital tract
Opportunistic pathogens

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9
Q

Corynebacterium diphtheriae characteristics

A

Pleomorphic G+B with metachromatic granules

4 biotypes: belfanti, gravis, intermedius, mitis

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10
Q

Corynebacterium diphtheriae pathogenesis

A

Diphtheria toxin - major virulence factor, exotoxin produced at site of infection and spreads thru blood to produce systemic symptoms

Coded for by tox gene which enters organism via lysogenic phage
Classic A-B toxin

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11
Q

Corynebacterium diphtheriae clinical disease

A

Diphtheria: clinical presentation is determined by site of infection, immune status of patient, virulence of organism

Respiratory: malaise, sore throat, fever, exudative pharyngitis that develops into thick pseudomembrane (adheres to underlying tissue), systemic illness in severe cases: myocarditis, congestive heart failure, cardiac arrhythmias

Cutaneous: acquired through skin contact, papule develops turning into chronic non-healing ulcer

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12
Q

Corynebacterium jeikeium characteristics

A

Opportunistic pathogen in immuno-compromised pt. and hospitalized pts.

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13
Q

Corynebacterium urealyticum

A

Urinary tract pathogen, immunosuppressed, genitourinary disorders, previous urological procedures, or antibiotic therapy.

Produces urease which makes urine alkaline –> renal stones

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14
Q

Corynebacterium pseudotuberculosis and ulcerans

A

Both closely related to diphtheriae
Can carry diphtheria gene
Pseudotuberculosis infections are rare
Ulcerans causes same disease as diphtheria

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15
Q

Mycobacterium spp. characteristics

A

Acid fast bacilli, cell walls rich in lipids - mycolic acids - cells won’t decolorize
Provides resistance to many antibiotics, antigenicity, and clumping

Non-motile
Aerobic
Non-spore forming
Slow growth

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16
Q

Runyon Classification

A

For non-tuberculosis mycobacteria

Slow-growing photochromogens (pigment in exposure to light)

Slow-growing scotochromogens (pigment in absence of light)

Slow-growing non-pigmented

Rapidly growing

M. Tuberculosis complex - slow-growing non-pigmented or light tan color

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17
Q

Slow-growing photochromogens mycobacteria

A

M. kansasii

M. marinum

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18
Q

Slow-growing scotochromogens mycobacteria

A

Mycobacterium gordonae

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19
Q

Slow-growing non-pigmented mycobacteria

A

M. avium

M. intracellulare

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20
Q

Rapidly-growing mycobacteria

A

M. fortuitum
M. chelonae
M. abscessus

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21
Q

Mycobacterium tuberculosis

A

Intercellular pathogen taken into resp. tract
Phagocytize do by macrophages where it grows. Macrophages secrete TNF and IL-12 which bring on intercellular killing

Granulomas (necrotic mass trapping bacteria) are formed. A small one is killed. A large one be coated with fibrin which protect the bacteria from macrophage killing

Humans only known reservoir
Spread thru inhalation of infectious aerosols

22
Q

M. tb clinical disease

A

Most infections in middle to lower lungs, can be anywhere

Diagnosis with x-ray and positive PPD skin test

23
Q

Neisseria spp. Characteristics

A 
G-DC (kidney beans) 
Aerobic
OXI+
CAT+
Oxidize carbs
Non-fermenters
Non-motile 
Non-spore forming
24
Q

Neisseria gonorrhoae characteristics

A 
G-DC
Oxidize glucose (g)
Fastidious - require cystine
CO2
MTM media
25
Q

Neisseria meningitidis characteristics

A

G-DC

Oxidize glucose and maltose (g,m)

26
Q

Neisseria structure

A

G- cell wall

N. meningitidis - polysaccharide capsule - allows for antigenic aero typing (A, B, C, Y,
N. gonorrhoae lacks a capsule

Pili - attachment and conjugation (pathogenicity and virulence)

Por A and B integral proteins - virulence factor that interferes with phagolysosome fusion
(gonorrhoae only has Por B)

OPA proteins - membrane proteins that mediate binding to epithelial and phagocytic cells; cell-cell signaling - clinical disease and virulence

27
Q

Mycobacterium leprae characteristics and clinical presentation

A

slow replication, long incubation period
symptoms can develop 20 yrs. after infection

2 kinds: tuberculoid leprosy - strong cellular response, lymphs and granulomas, few bacteria, cytokines induced, macrophages, phagocytosis, bacillary elimination

lepromatous leprosy - strong Ab response, no cellular, many bacteria in dermal macrophages and peripheral nerve Schwann cells * most infectious form

person-person spread
lepromin skin test - injection of inactivated leprosy bacillus under skin to detect infection

28
Q

Mycobacterium leprae clinical disease

A

leprosy - chronic infection affecting skin and peripheral nerves, disease is host response

tuberculoid - milder, hypo pigmented skin macules, less organisms

lepromatous - disfiguring skin lesions, nodules, plaques, thickened dermis, involvement of nasal mucosa, more bacteria

29
Q

Mycobacterium avium/MAC

A

MAC - Mycobacterium avium complex

disease in immunocompromised

pulmonary disease seen in immune-competent pts.

tons of bacteria

ingestion of bacteria, not person-person, contaminated aerosols

replication in localized lymph nodes, then systemic spread

30
Q

Enterobacteriaceae characteristics

A 
G-B
FA
CAT+
OXI-
ferment glucose
reduce nitrate
no spores
soil, water, vegetation, normal flora
peritrichous pili if motile
fimbriae - adherence 
conjugative pili
31
Q

3 kinds of Enterobacteriaceae pathogens

A
  1. strict pathogens
    Salmonella Typhi, Shigella, Y. pestis
  2. Opportunistic pathogens
    K. pneumoniae, P. mirabilis
  3. Acquired virulence pathogens
    E. coli gastroenteritis (E. coli 0157)
32
Q

Enterobacteriaceae structure

A

LPS - major cell wall Ag, heat stable

Made up of outermost O polysaccharide, core polysaccharide, Lipid A

33
Q

3 antigen groups used for serological classification of Enterobacteriaceae

A
  1. Somatic O polysaccharides
  2. Capsular K antigens (block O polysaccharide, heat-labile)
  3. Flagellar H proteins (present in motile pathogens, heat-labile)
34
Q

3 virulence factors of Enterobacteriaceae

A
  1. Capsule - avoid phagoctosis
  2. Endotoxin - Lipid A, activate complement, cytokine release, leukocytosis, thrombocytopenia, DIC, shock and death
  3. Type III secretion system - allow bacteria to secrete proteins into phagocyte –> destroys proteins needed for phagocytosis; suppresses cytosine production –> lowers inflammatory response and prevents complement binding
35
Q

ETEC

A

Enterotoxigenic E. coli

young children, travelers (water/food, high innoculum)

enterotoxin - Lipid A
genes on plasmid

need to colonize AND produce toxins to cause disease

36
Q

EPEC

A

Enteropathogenic E. coli

infants (daycare –> diapers)

person-person spread (lower innoculum)

pathogenicity island - regulates attachment and destruction

destruction of microvilli

37
Q

EAEC

A

Enteroaggregative E. coli

infants, travelers

auto-agglutinate - protection from Abs and phagocytosis

chronic, watery diarrhea

38
Q

EHEC

A

Enterohemorrhagic E. coli

most common strain

young children (can develop HUS - kidney failure)

from unpasteurized dairy, contaminated veggies, undercooked meat, chopped meat, apple juice

E. coli 0157 - acquire Shigella toxins via lysogenic bacteriophage

39
Q

EIEC

A

Enteroinvasive E. coli

invade and destroy colonic epithelium

very closely related to Shigella

Rare in the US

40
Q

Extraintestinal E. coli infections

A

UTI - adhesions prevent elimination via voided urine

Neonatal meningitis - infants <1 month, K1 capsular Ag, common in GI tracts of pregnant women and newborns

Septicemia 0 originates from GI or UT

41
Q

Salmonella Clinical Disease

A

Gastroenteritis - most common form of Salmonellosis, consumption of contaminated food
nausea, vomiting, cramps, diarrhea (no blood)

Septicemia

Typhoid fever - caused by S. typhi and a mild form by S. paratyphoid
macrophages transport bacteria to the liver, spleen,a dn bone marrow
fever, headache, myalgias, malaise, anorexia
chronic colonization
humans only

42
Q

Shigella

A

4 spp.

bacillary dysentery
invasive - colon lining, adherence, invasion, replication (genes and plasmid)

dysenteric strains - enterotoxic Shigella toxin - causes diarrhea (A-B)
Renal failure

only humans, mostly children
person-person spread

abdominal cramps, fever, watery diarrhea, increased WBC count, blood and pus in stool

43
Q

Yersinia pestis

A

Plague: urban plague - rats from fleas

sylvatic plague - squirrles, rabbits, field rats, domestic cats

2 plasmids coding for virulence genes:
F1 - antiphagocytic protein
Plasminogen activator protease gene - degrades complement, preventing opsonization and phagocytosis; degrades fibrin clots –> spread

Clinical disease:
bubonic plague - bitten by infected flea, fever and painful bubos, bacteremia

Pneumonic plague - fever, malaise, pulmonary signs, highly infectious aerosol

44
Q

Yersinia enterocolitica

A

Enteric pathogen

enterocolitis - diarrhea, fever, abdominal pain, can mimic appendicitis

blood transfusion-related bacteremia and endotoxic shock

45
Q

Yersinia spp.

A

Y. pestis
Y. enterocolitica

Type III secretion system

ALL infections are zoonotic

46
Q

Klebsiella

A

prominent capsule - mucoid colonies

K. pneumoniae and K. oxytoca - community and nosocomial lobar pneumonia; also wound, soft tissue, UTI

K. granulomatis - granuloma inguinale –> called donovanosis
subcutaneous nodules develop into painless granulomatous lesions that can extend out and coalesce. STI or via genital trauma

47
Q

Proteus

A

P. mirabilis - most common
UTI, produces urease which makes urine alkaline –> renal stones
produce fimbria for adherence

48
Q

Campylobacter Characteristics

A 
G-B spiral-shaped (not spirilium!) 
Microaerophilic (CO2)
No fermentation or oxidation of carbs
Polar flagella
25 spp.

G- cell wall, LPS major cell wall Ag
Somatic O polysaccharide, heat-labile capsular and flagellar Ags.

49
Q

Helicobacter Characteristics

A 
G-B spiral-shaped (not spirilium!)
Microaerophilic (CO2)
No fermentation or oxidation of carbs
Most OXI+
Most CAT+
Ferment amino acids
50
Q

Campylobacter Diseases

A

Gastroenteritis - C. jejuni or C. coli
an acute enteritis with diarrhea, fever, abdominal pain, bloody stool, chronic in immunocompromised

Septicemia/systemic infections (arthritis, septic abortion) - C. fetus

51
Q

Campylobacter jejuni

A

Adhesins, cytotoxic enzymes, enterotoxins 0 not only cause of virulence (strains lacking these are still virulent)

Seen in pts. undergoing treatment for gastric acids

GI disease - ulcerated, edematous, bloody crypt abcesses

52
Q

Campylobacter fetus

A

heat-stable capsule-like protein (S protein) - prevents complement binding –> only virulence factor

53
Q

Helicobacer pylori

A 
G-B spiral (not spirilium!)
polar flagella - highly motile
urease
OXI+
CAT+
ferment amino acids
LPS - lipid A low endotoxin activity 
CAUSE ULCERS

Clinical Microbiology Lecture (19 decks)

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