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Pathogenic Microbiology > Test 3 > Flashcards

Test 3 Flashcards

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1
Q

Describe the Pseudomonas genus and other related genera

A

Nonfermentive rods, opportunistic pathogens, arranged in pairs of cells that resemble a single cell; found in soil, decaying organic matter, vegetation, water, and hospital environments; simple growth requirements, use many organic compounds as sources of carbon and nitrogen, resistant to common antibiotics, primarily opportunistic

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2
Q

Describe Pseudomonas aeruginosa

A

Motile, straight or slightly curved, gram negative rods in pairs, obligate aerobes, have cytochrome oxidase, appear mucoid due to capsule, and can produce diffusible pigments

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3
Q

What are the virulence factors of Pseudomonas aeruginosa

A

Adhesins (mucoid alginate), toxins (Exotoxin A, pyocyanin, etc.), and enzymes (elastases, phospholipase C), and a type III Secretion System

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4
Q

Describe how Exotoxin A in Pseudomonas aeruginosa impacts cells

A

It disrupts protein synthesis by blocking peptide chain elongation in eukaryotic cells

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5
Q

What diseases does Pseudomonas aeruginosa cause?

A

Infections of the lower respiratory tract ranging from asymptomatic colonization to necrotizing bronchopneumonia, primary skin infections (burn wounds, folliculitis, osteochrondritis, etc.), UTIs, ear infections, eye infections, bacteremia, endocarditis, and more.

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6
Q

How should Pseudomonas aeruginosa be diagnosed and treated?

A

Gram negative rods in pairs, required aerobic incubations, positive oxidase reactions, B-hemolysis, a green pigmentation due to pyocyanin, a sweet grapelike odor, and resistance to broad spectrum antibiotics

Treatment should be with a combination of active antibiotics and NO B-lactams

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7
Q

Generally describe the Burkholderia genus

A

Opportunistic pathogens, colonize a variety of moist environmental surfaces, susceptible to trimethoprim-sulfamethoxazole (TMP-SMZ)

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8
Q

Describe the facets of the species Burkholderia cepacia, B. pseudomallei, and B. mallei

A

B. cepacia: Respiratory tract infections, opportunistic infections

B. pseudomallei: Bioweapon, causes pulmonary disease ranging from bronchitis to necrotizing pneumonia

B. mallei: Glanders (ulcerating nodules in lungs) in livestock

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9
Q

Describe Stenotrophomonas maltophilia

A

Causes infections (bacteremia, pneumonia, etc.) in debilitated patients with impaired host defense mechanisms, resistant to commonly used B-lactams, aminoglycosides, and carbapenems; treat by trimethoprim-sulfamethoxazole (TMP-SMZ)

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10
Q

Describe Acinetobacter as a genus

A

Strictly aerobic, oxidase negative, plump gram negative coccobacilli; saprophytes, recovered in nature and in the hospital, survive on moist surfaces and dry surfaces, part of the normal oropharyngeal flora; subdivided into glucose oxidizing and glucose nonoxidizing; opportunistic pathogens, infect the respiratory and urinary tracts, and can infect wounds; treated by broad spectrum antibiotics

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11
Q

Describe Moraxella catarrhalis

A

Strictly aerobic, oxidase positive, gram negative diplococci, common cause of bronchitis and bronchopneumonia, sinusitis, and otitis; most produce B-lactamases and are resistant to penicillins

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12
Q

Describe the Haemophilus genus

A

Gram negative rods on mucous membranes of humans, sometimes pleomorphic, usually requires supplementation of media with hemin and/or NAD, some have a polysaccharide capsule and/or a serotype/biotype

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13
Q

What diseases do Haemophilus cause?

A

Ear infections, sinusitis, bronchitis, pneumonia, meningitis, epiglottitis, cellulitis, conjunctivitis, chancroid, etc.

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14
Q

What is the major virulence factor for Haemophilus influenzae type B?

A

The antiphagocytic polysaccharide capsule (made of polyribitol phosphate (PRP)), lipid A LPS component, and IgA protease

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15
Q

How should species of Haemophilus be collected and isolated/diagnosed?

A

Taking samples from the oropharynx, blood from patients, CSF cultures, antigen detection of the PRP capsular antigen, and growth of cultures on chocolate agar with hemin and/or NAD (also growth of satellite colonies around S. aureus on blood agar)

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16
Q

How should Haemophilus influenzae infections be treated?

A

Broad spectrum cephalosporins for severe infections, amoxicillin or fluoroquinolone for less severe infections, and immunization with purified capsular PRP (rifampin prophylaxis can be done for children at high risk)

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17
Q

Describe the two species Aggregatibacter actinomycetemcomitans and Aggregatibacter aphrophilus (also say the similarities between them)

A

A. actinomycetemcomitans: Causes periodontitis, endocarditis, and bite wound infections

A. aphrophilus: Causes endocarditis and opportunistic infections

Both colonize the human mouth and can spread into the blood (grow slowly in blood)

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18
Q

Describe the two species Pasteurella multocida and Pasteurella canis (also say the similarities between them)

A

P. multocida: Causes bite wound infections, chronic pulmonary disease, bacteremia, and meningitis (caught from cats or dogs); grows poorly on media selective for gram negative rods, treat with penicillin

P. canis: Causes bite wound infections (caught from dogs)

Both are small, facultatively anaerobic, fermentative coccobacilli found in the oropharynx of healthy animals; have a polysaccharide capsule made of hyaluronic acid

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19
Q

Describe the genus Bordetella

A

Extremely small, strictly aerobic, gram negative coccobacillus, four species cause human disease

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20
Q

What are the four species of Bordetella that cause disease and what are they best known for?

A

Bordetella pertussis: Pertussis or whooping cough
Bordetella parapertussis: A milder form of pertussis
Bordetella bronchiseptica: Respiratory disease in dogs, swines, lab animals, etc.
Bordetella holmesii: Uncommon cause of sepsis

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21
Q

What are the virulence factors for Bordetella pertussis?

A

Attachment is mediated by protein adhesins (pertactin, filamentous hemagglutinin, and fimbria), localized tissue damage mediated by dermanecrotic toxin and tracheal cytotoxin, and systemic toxicity produced by pertussis toxin (inactivates the protein that controls cAMP levels to increase mucus production in the respiratory system)

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22
Q

Describe the disease Pertussis

A

Human disease with human reservoir, used to be considered a pediatric disease but infections are also found in adolescents and adults, infection is initiated by aerosols and subsequent proliferation of the bacteria on ciliated epithelial cells

23
Q

What are the three stages (other than infection) of Pertussis?

A

Catarrhal stage: Resembles a common cold (sneezing, malaise, anorexia, low-grade fever), pose a high risk for spreading the disease
Paroxysmal stage: Clearance of mucus is impaired, classic whooping cough paroxysms begin
Convalescent stage: Paroxysms diminish in number and severity, but secondary complications are more likely, may not occur with people who have partial immunity or in adults

24
Q

What is the best way to diagnose B. pertussis?

A

Bacteria extremely sensitive to drying, must be supplemented with charcoal, starch, blood, or albumin to absorb toxic substances and metabolites, nucleic acid amplification assays or multiplex assays are the diagnostic test of choice

25
Q

How should infections of B. pertussis be treated?

A

Macrolides (erythromycin, etc.) are effective, trimethoprim-sulfamethoxazole can also be used, and two acellular vaccines are available (DtAP) for adults and children

26
Q

Generally describe the Campylobacter genus

A

Motile, comma-shaped gram negative rods, 4 species are common human pathogens, grow best in reduced oxygen and increased carbon dioxide, express lipooligosaccharides (LOS), zoonotic infections

27
Q

What are the 4 pathogenic species of Campylobacter, and what are the specific diseases/attributes for each one?

A

C. jejuni: Bacterial gastroenteritis; grows better at 42 degrees than at 37 degrees, produces histologic damage to the mucosal surfaces of the jejunum, associated with Guillain-Barre syndrome, obtained by consumption of contaminated food/milk/water

C. coli: Less common, bacterial gastroenteritis; obtained by consumption of contaminated food/milk/water

C. upsaliensis: ~10% of bacterial gastroenteritis; associated with Guillain-Barre syndrome, obtained by contact with domestic dogs, not isolated by commonly used techniques

C. fetus: Systemic infections such as bacteremia, septic thrombophlebitis, arthritis, septic abortion, and meningitis; commonly spreads from the GI tract to the blood and distal foci, resistant to complement and antibody-mediated serum killing, covered with a heat stable capsule-like protein (S protein)

28
Q

What are the diseases that can be caused by Campylobacter species?

A

Acute enteritis (diarrhea, fever, severe abdominal pain), GI infections, Guillain-Barre syndrome (autoimmune disease), and reactive arthritis

29
Q

How should Campylobacter be diagosed?

A

S-shaped organisms in a stool specimen, commercial immunoassays, nucleic acid based tests, growth in microaerophilic atmosphere at an elevated incubation TM, and extended culturing time (slow growing)

30
Q

How should Campylobacter infections be treated?

A

Gastroenteritis is typically self-limiting, severe infections or septicemia can use tetracyclines, chloramphenicol, fluoroquinolones, etc.; avoid infections by proper food perpartion, etc.

31
Q

Describe the genus Helicobacter

A

Spiral gram-negative rods, primarily colonize the stomach or intestines, highly motile (corkscrew motility), produce an abundance of urease, catalase and oxidase positive, do not ferment or oxidize carbohydrates, require a complex medium supplemented with blood, serum, charcoal, starch, or egg yolk in microaerophilic conditions

32
Q

What diseases does Helicobacter pylori cause, what is the natural reservoir, and how do infections spread?

A

Gastritis, peptic ulcers, gastric adenocarcinoma, and MALT B-cell lymphomas; humans are the primary reservoir, and the fecal-oral route is the way infections are spread

33
Q

What are the virulence factors/pathogenesis factors for Helicobacter pylori?

A

Initial colonization by blockage of acid production by a bacterial acid-inhibitory protein and neutralization of gastric acids, localized tissue damage (urease by-products, mucinase, phospholipases, and VacA), the type VI secretion system encoded the cagA gene, and IL-8 production by PAI genes to attract neutrophils

34
Q

How should infections of Helicobacter pylori be diagnosed?

A

Examination of gastric biopsy specimens or antigen detection (generally noninvasive assays are done rather than culturing)

35
Q

How should infections of Helicobacter pylori be treated?

A

Proton pump inhibitors with a macrolide and B-lactam have been the best for treatment so far

36
Q

What are the four species of Brucella?

A

B. abortus (mild disease), B. melitensis (severe disease), B. suis (formation of destructive lesions), and B. canis (mild disease)

37
Q

Generally describe the Brucellae genus

A

Small, nonmotile, nonencapsulated, gram negative coccobacilli, slow growing, require complex growth media, strict aerobes, and does not ferment carbohydrates, and intracellular parasite of the reticuloendothelial system, worldwide distribution of the bacteria

38
Q

What are the virulence factors of Brucellae?

A

No endotoxin, the O chain of the smooth LPS

39
Q

How are Brucella infections obtained?

A

Direct contact with the organism, ingestion of contaminated food products, inhalation

40
Q

What are the symptoms of Brucella infections?

A

Infection in organs rich in erythritol, acute disease with malaise, chills, sweats, fatigue, weakness, and undulant fever etc., advanced disease with gastrointestinal tract symptoms, and chronic infections with relapses common

41
Q

How should Brucella be diagnosed?

A

Several blood samples for culture and serological testing, bone marrow and infected tissue cultures, incubation of blood cultures for 2 weeks for confirmed negative results; preliminary positives include: positive oxidases and urease reactions, reactivity with specific antibodies, microscopic and colonial morphology, and sequencing of 16s rRNA

42
Q

How should Brucella infections be treated?

A

Tetracyclines with doxycycline (bacteriostatic, so relapses common), or doxycycline with rifampin, animal vaccination, elimination of infected herds, and avoidance of risk factors

43
Q

Generally describe Francisella tularensis (most common diseases causing in the genus)

A

Zoonotic pathogen, very small, faintly staining, gram negative coccobacillus, nonmotile, thin lipid capsule, fastidious growth requirements (cysteine) strictly aerobic, intracellular pathogen, replicates in immune cells, and polysaccharide-rich capsule that is antiphagocytic

44
Q

What diseases does F. tularensis cause?

A

Tularemia (glandular fever, rabbit fever, tick fever, or deerfly fever) that can be ulceroglandular, oculoglandular, typhoidal, pneumonic, gastrointestinal, or oropharyngeal

45
Q

How should tularemia infections be diagnosed and treated?

A

Diagnosis: Nucleic acid amplification tests, growth on chocolate agar or buffered charcoal yeast extract (BCYE) agar with cysteine, watching for growth of small gram-negative coccobacilli on chocolate agar, and reaction with specific antiserum, and increase of antibody titers in the body

Treatment: Gentamicin is best choice, doxycycline and ciprofloxacin for mild infections, and not B-lactams; avoid vectors of infection like ticks

46
Q

Generally describe Legionella pneumophila

A

Gram negative rod, does not grow on common laboratory media, stains poorly, slender, pleomorphic, long on media, obligate aerobes, nutritionally fastidious (cysteine and iron), facultative intracellular bacteria that multiply in alveolar macrophages, and have worldwide distribution in natural/human made bodies of water

47
Q

What are the symptoms of Pontiac fever or legionnaires disease?

A

Pontiac Fever: Fever, chills, myalgia, malaise, headache, spontaneous resolving of the disease without antibiotics

Legionnaires disease: More severe, acute symptoms after 2-10 days of incubation, multi-organ disease, pneumonia and multilobar consolidation and inflammation, and declining pulmonary function throughout the disease

48
Q

How are infections of L. pneumophilia diagnosed and treated?

A

Diagnosis: Microscopy, culturing, and serology, immunoassays for the specific antigens (LPS antigen), and nucleic acid amplification assays, growth of long bacteria on media with L-cysteine and iron

Treatment: Macrolides or fluoroquinolones, not B-lactams since they do not penetrate macrophages

49
Q

Generally describe the anaerobic gram negative rods genus Bacteroides

A

Predominant on mucosal surfaces, B. fragilis is most important member, growth is stimulated by bile, pleomorphic in size and shape, stain weakly, grow rapidly in culture, surrounded by a polysaccharide capsule

50
Q

What are the pathogenic factors of B. fragilis?

A

Fimbriae to adhere to cells, antiphagocytic polysaccharide capsule, short chain fatty acids produced during anaerobic metabolism, proteases, catalase and superoxide dismutase, and a heat-labile zinc metalloprotease toxin

51
Q

What diseases does B. fragilis cause?

A

RT infections, brain abscesses, intraabdominal infections, gynecologic infections, skin and soft-tissue infections, bacteremia, and gastroenteritis

52
Q

How is B. fragilis diagnosed and treated?

A

Diagnosis: Microcopy, anaerobic culturing, moist culture conditions, rapid growth, bile supplementation, and 16S rRNA sequencing

Treatment: Antibiotic therapy combined with surgical intervention, no B-lactams, metronidazole, carbapenems, and B-lactam-B-lactamases inhibitors

53
Q

Generally describe the Fusobacterium genus

A

Obligate gram negative anaerobe, fusiform, non-spore former, non-hemolytic, lecithinase and indole positive

54
Q

What are the diseases caused by Fusobacterium necrophorum, what are the symptoms, and what are the treatments?

A

Lemierre’s syndrome (occurs after prolonged or severe pharyngitis, can enter lungs by aspiration, blood clots in the lungs)

Treat with carbapenems and metronidazole

Pathogenic Microbiology (4 decks)

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