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Clinical Microbiology Lecture > Exam 2 > Flashcards

Exam 2 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
Neisseria gonorrhoae characteristics
``` G-DC Oxidize glucose (g) Fastidious - require cystine CO2 MTM media ```
25
Neisseria meningitidis characteristics
G-DC | Oxidize glucose and maltose (g,m)
26
Neisseria structure
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
Mycobacterium leprae characteristics and clinical presentation
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
Mycobacterium leprae clinical disease
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
Mycobacterium avium/MAC
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
Enterobacteriaceae characteristics
``` 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
3 kinds of Enterobacteriaceae pathogens
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
Enterobacteriaceae structure
LPS - major cell wall Ag, heat stable Made up of outermost O polysaccharide, core polysaccharide, Lipid A
33
3 antigen groups used for serological classification of Enterobacteriaceae
1. Somatic O polysaccharides 2. Capsular K antigens (block O polysaccharide, heat-labile) 3. Flagellar H proteins (present in motile pathogens, heat-labile)
34
3 virulence factors of Enterobacteriaceae
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
ETEC
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
EPEC
Enteropathogenic E. coli infants (daycare --> diapers) person-person spread (lower innoculum) pathogenicity island - regulates attachment and destruction destruction of microvilli
37
EAEC
Enteroaggregative E. coli infants, travelers auto-agglutinate - protection from Abs and phagocytosis chronic, watery diarrhea
38
EHEC
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
EIEC
Enteroinvasive E. coli invade and destroy colonic epithelium very closely related to Shigella Rare in the US
40
Extraintestinal E. coli infections
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
Salmonella Clinical Disease
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
Shigella
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
Yersinia pestis
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
Yersinia enterocolitica
Enteric pathogen enterocolitis - diarrhea, fever, abdominal pain, can mimic appendicitis blood transfusion-related bacteremia and endotoxic shock
45
Yersinia spp.
Y. pestis Y. enterocolitica Type III secretion system ALL infections are zoonotic
46
Klebsiella
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
Proteus
P. mirabilis - most common UTI, produces urease which makes urine alkaline --> renal stones produce fimbria for adherence
48
Campylobacter Characteristics
``` 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
Helicobacter Characteristics
``` G-B spiral-shaped (not spirilium!) Microaerophilic (CO2) No fermentation or oxidation of carbs Most OXI+ Most CAT+ Ferment amino acids ```
50
Campylobacter Diseases
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
Campylobacter jejuni
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
Campylobacter fetus
heat-stable capsule-like protein (S protein) - prevents complement binding --> only virulence factor
53
Helicobacer pylori
``` 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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