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Infectious Disease 1 > Exam Review 2 > Flashcards

Exam Review 2 Flashcards

1
Q

What UTIs can occur in the upper urinary tract?

A

Pyelonephritis, intra-renal abscess; Perinephric abscess (usually late complications of pyelonephritis)

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2
Q

What UTIs can occur in the lower urinary tract?

A

Cystitis; Urethritis; Prostatitis

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3
Q

What is an uncomplicated UTI?

A

Infection in a structurally and neurologically normal urinary tract in otherwise healthy patients

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4
Q

What is a complicated UTI?

A

Infection in a urinary tract with functional or structural abnormalities (e.g. indwelling catheters and renal calculi); Infection in patients with an underlying condition that increases risk of treatment failure (diabetes, immunosuppression, indwelling bladder catheter)

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5
Q

What are symptoms of cystitis?

A

Dysuria, urinary urgency and frequency, bladder fullness/discomfort; NOTE: Hemorrhagic cystitis (bloody urine) reported in as many as 10% of cases of UTI in otherwise healthy women

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6
Q

What are symptoms of pyelonephritis?

A

Fever, sweating, nausea, vomiting, flank pain & pain in the costovertebral areas, dysuria, urinary frequency and urgency; if there is systemic involvement, there can be signs and symptoms of dehydration, hypotension

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7
Q

Who is at risk of renal abscess with UTI?

A

patients with urinary tract abnormalities, diabetic patients

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8
Q

What are symptoms of UTI in children

A

enuresis, fever, poor weight gain

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9
Q

How should a UTI be diagnosed?

A

Urinalysis: microscopic examination of urine (Presence of WBC (pyuria), RBC, bacteria); Urine dipstick test: rapid screening test (leukocyte esterase test to test for pyuria, Nitrate ® nitrite test (+ve in only 25%))

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10
Q

What is the gold standard for diagnosing UTI?

A

Microbiological analysis: Bacterial count >10^5 cfu/ml regarded as significant

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11
Q

When should a urine sample be cultured?

A

Pyelonephritis and complicated UTIs, Children, pregnant women, Patients with structural abnormalities of the urinary tract, men

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12
Q

Who should be screened for asymptomatic UTI?

A

Pregnant women, Patients undergoing urologic surgery, transurethral resection of prostate

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13
Q

What is the usual cause of UTI?

A

E. Coli!!! Sometimes S. saprophyticus

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14
Q

What are risk factors for UTI in women?

A

Short urethra, Sexual intercourse & lack of post coital voiding, Diaphragm, spermicide use, Pregnancy, Disruption of normal bacterial flora

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15
Q

What are UTI virulence factors?

A

Enhanced adherence to receptors on uroepithelial cells (Type 1 fimbriae and P fimbriae - pili!), flagella (enhanced motility), Production of hemolysin, Production of aerobactin (a siderophore, which allows for iron acquisition)

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16
Q

What are symptoms of acute bacterial prostatitis?

A

Symptoms similar to lower tract infection, Fever, perineal and back pain, Urinary retention (edema of prostate)

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17
Q

What findings are common in bacterial prostatitis?

A

Warm, swollen, tender prostate on rectal exam; Abnormal urinalysis with pyuria (WBC), positive urine culture, blood culture may be positive

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18
Q

What is treatment for bacterial prostatitis?

A

Treatment consists of LONGER course of antibiotics and pain control (NSAIDS)

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19
Q

What are the common treatments for UTIs?

A

Short course (3-day) therapy for uncomplicated infections; Longer duration (10-14 days) for complicated infection (e.g. pyelonephritis); Oral vs. intravenous agents (TMP/SMX, nitrofurantoin, Fluoroquinolones) - depends on tolerance/nausea

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20
Q

What are the risk factors for recurrent UTI?

A

Postmenopausal status; diabetes; Recent antimicrobial use; Behavioral risk factors (Frequency of sexual intercourse, Spermicide use, New partner, First UTI

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21
Q

When should UTI prophylaxis be given?

A

> 2 symptomatic UTIs within six months or >3 over 12 months

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22
Q

What are plasmids?

A

Extrachromosomal, Circular or linear, 2 kb to hundreds of kb in size, Non-essential, May carry ‘supplemental’ genetic information or may be cryptic, Employ host functions for most of DNA metabolism

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23
Q

What are insertion elements?

A

Simplest type of transposable element found in bacterial chromosomes and plasmids, Encode only genes for mobilization and insertion, Range in size from 768 bp to 5 kb, IS1 first identified in E. coli’s glactose operon is 768 bp long and is present with 4-19 copies in the E. coli chromosome, Ends of all known IS elements show inverted terminal repeats (ITRs).

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24
Q

What is transformation?

A
  1. Lysis of donor cell releases DNA into medium; 2. Donor DNA is taken up by recipient
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25
Q

What is conjugation?

A

Donor DNA is transferred directly into recipient through a connecting tube. Contact and transfer and promoted by a specialized plasmid in the donor cell.

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26
Q

What is transduction?

A
  1. Bacteriophage infects a cell; 2. Lysis of donor cell. Donor DNA is packaged and released into the bacteriophage; 3. Donor DNA is transferred when phage particle infects recipient cell.
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27
Q

What is R-plasmid conjugation?

A
  1. The bacterium with an R-plasmid is multiple antibiotic resistant and can produce a sex pilus (serve as a genetic donor). 2. The sex pilus adheres to an F- female (recipient). One strand of the R-plasmid breaks. 3. The sex pilus retracts and a bridge is created between the two bacteria. One strand of the R-plasmid enters the recipient bacterium. 4. Both bacteria make a complementary strand of the R-plasmid and both are now multiple antibiotic resistant and capable of producing a sex pilus.
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28
Q

How can you inhibit transformation?

A

DNAase

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29
Q

How can you inhibit conjugation?

A

Physical barrier

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30
Q

For which bacteria is transduction important for resistance?

A

Vibrio cholera, Corynebacterium diphtheriae, Neisseria meningitidis

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31
Q

For which bacteria is conjugation important for resistance?

A

Bacillus spp.

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32
Q

What is pseudomonas aeruginosa and where is it found?

A

It’s an opportunistic pathogen found in soil, salad bars, shower heads; it causes disease in impaired hosts (VAP, CF); gram neg rods

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33
Q

What are common virulence factors?

A

Pili (fimbriae) - attachment; Siderophores - iron scavenging; Flagella - motility; LPS - immune system stimulation; Type III secretion system - toxins; biofilm

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34
Q

What does TLR5 recognize?

A

Flagella; only responds to invasive organisms; proinflammatory and participates in NFkB pathway; polymorphisms in TLR5 affect disease susceptibility; Activates the NLRC3 inflammasome – causes pathology

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35
Q

What pathway is TLR4 involved in?

A

JAK/STAT; recognizes LPS; Type I IFN

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36
Q

Where does LPS come from?

A

Gram negatives; actively shed from growing organisms, released from lysed – dying bacteria

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37
Q

What virulence factors does P. aeruginosa express?

A

Expression of flagella, pili, type III toxins

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38
Q

How do bacteria “communicate”?

A

Homoserine lactones (small highly diffusable molecules), Cyclic di GMP; Secretion of small molecules – taken up by surrounding organisms – along with a transcriptional activator – initiate gene expression in the “community”

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39
Q

How does P. aeruginosa avoid the immune system?

A

Biofilm mode of growth; loss of flagella (loss of motility);

LPS mutations – loss of the O-side chains; Lack of type III toxin expression

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40
Q

What are obligate anaerobes?

A

Unable to grow if > than 0.5% oxygen

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41
Q

What are moderate anaerobes?

A

Capable of growing between 2-8% oxygen

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42
Q

What are Microaerophillic bacteria?

A

Grows in presence of oxygen, but better in anaerobic conditions

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43
Q

What are Facultative bacteria (facultative anaerobes)?

A

Grows both in presence and absence of oxygen

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44
Q

Why can’t anaerobic bacteria function in oxygen?

A

They metabolize the oxygen, produce toxic byproducts, can’t detox, bacteria die

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45
Q

What does bacteroides fragilis do normally in host?

A

synthesizes vitamin K and deconjugates bile acids

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46
Q

What do anaerobic bacteria normally contribute to host?

A

Fermentation of undigested carbohydrates, Training immune system, Roles evaluated in disease states (obesity, inflammatory bowel disease, cancer etc)

47
Q

What are common anaerobes?

A

Gram + bacilli: Clostridium perfringens, tetani, botulinum, difficile, Actinomyces, p. acnes; Gram - bacilli: Bacteroides fragilis, thetaiotaomicron

48
Q

What do anaerobic cocci do to the body?

A

Brain abscesses, periodontal disease, pneumonias, skin and soft tissue infections, intra-abdominal infections; P. magnus: chronic bone and joint infections, especially prosthetic joints; P. prevotti and P. anaerobius: female genital tract and intra-abdominal infections

49
Q

Which gram + anaerobes create spores?

A

Clostridium (C. perfringens, C. difficile, C. tetani, C. botulinum)

50
Q

What is proprionibacterium?

A

Produces propionic acid as major byproduct of fermentation; Colonize skin, conjunctiva, external ear, oropharynx, female GU tract; P. acnes; Prosthetic devices (heart valves, ventricular shunts); virulence is low - “infection” occurs much later; non-spore forming gram + bacilli

51
Q

What is clostridium?

A

Ubiquitous - Present in soil, water, sewage, normal flora in GI tracts of animals and humans; forms spores, resistant to heat, dessication, and disinfectants, can survive for years in adverse environments; Toxin elaboration (histolytic toxins, enterotoxins, neurotoxins)

52
Q

What is Clostridium perfringens?

A

GI tract of humans and animals; Type A responsible for most human infections, is widely distributed in soil and water contaminated with feces; Self-limited gastroenteritis, soft tissue infections: cellulitis, fascitis or myonecrosis (gas gangrene)

53
Q

What is Clostridial myonecrosis?

A

Caused by perfringens; Symptoms begin 1-4 days after inoculation and progresses rapidly to extensive muscle necrosis and shock; Local area with marked pain, swelling, serosanguinous discharge, bullae, slight crepitance; Treated with Surgical debridement, Antibiotics, Hyperbaric oxygen

54
Q

What causes C diff?

A

Antibiotic exposure associated with overgrowth of C. difficile; Enterotoxin (toxin A) produces chemotaxis, induces cytokine production and hypersecretion of fluid, development of hemorrhagic necrosis; Cytotoxin (toxin B) induces polymerization of actin with loss of cellular cytoskeleton

55
Q

How do you treat C diff?

A

Discontinue antibiotics, Metronidazole (PO or IV) or vancomycin (PO) are treatments of choice, Fecal microbial transplant (FMT); NOTE: Relapse in 20-30% (spores are resistant; imbalanced colonic flora)

56
Q

What is Clostridium tetani?

A

Disease in un-vaccinated or inadequately immunized (disease does not induce immunity); Spore (found in soil, GI tract of animals) inoculated into wound; Tetanospasmin (heat-labile neurotoxin) blocks release of inhibitory neurotransmitters (eg. GABA) into synapses, allowing excitatory synapses to be unregulated. This results in muscle spasms - binding is irreversible

57
Q

What are symptoms of tetanus?

A

Trismus (lock jaw), risus sardonicus (contraction of facial muscles), Sweating, hyperthermia, cardiac arrythmias, labile blood pressure; can cause infection in umbilical stump or twisting of cord

58
Q

How is tetanus treated?

A

Debridement of wound, Metronidazole, Tetanus immunoglobulin, Vaccination with tetanus toxoid

59
Q

What is Clostridium botulinum?

A

Blocks neurotransmission at peripheral cholinergic synapses, Prevents release of acetylcholine, resulting in muscle relaxation; can get foodborne botulism or infant botulsim (from spores)

60
Q

What is the difference between foodborne and infant botulism?

A

Foodborne: consumption of preformed toxin; Infant: Disease associated with neurotoxin produced in vivo

61
Q

What are symptoms of botulism?

A

Symmetric cranial nerve palsies (III, IV, VI, VII) causing 4Ds: diplopia, dysphonia, dysarthria, and dysphagia; Symmetric flaccid paralysis

62
Q

How is botulism treated?

A

Supportive care, Elimination of organism from GI tract (Gastric lavage, Metronidazole or penicillin); Botulinum Immunoglobulin (BIG): pooled plasma from adults immunized with pentavalent (ABCDE) botulinum toxoid

63
Q

How is S. pneumonia treated - in peds? In adults?

A

Peds: Beta-lactam antibiotics (PCN - ampicillin) or cephalosporins (ceftriaxone); adults: macrolide (azithromycin), if co-morbidity: fluoroquinolone or beta-lactam plus macrolide

64
Q

What is mycoplasma?

A

Does not have a cell wall - Cell membrane contains sterols not present in other bacteria; diagnosis usually by serology (IgG); TLR2 important for binding to respiratory epithelium; Remains extracellular; Acts as a super antigen stimulating PMNs and macrophages to release cytokines; Causes local destruction of cilia, interferes with normal airway clearance which leads to mechanical irritation and persistent cough

65
Q

What is “walking pneumonia”?

A

Mycoplasma - lacks seasonal pattern, spread by droplet secretions

66
Q

Who gets mycoplasma?

A

children and young adults

67
Q

What are symptoms of mycoplasma?

A

Mild respiratory symptoms

68
Q

How do you treat mycoplasma?

A

Macrolides (erythromycin, azithromycin, clarithromycin), Fluoroquinolones (levofloxacin)

69
Q

What are Chlamydophila pneumonias?

A

Infect non-ciliated columnar cells, Multiply in alveolar macrophages, Perivascular and peribronchiolar infiltrates, Clinical symptoms due to host immune response

70
Q

What is C. trachomatis pneumonia?

A

Neonatal infection presents at 1-3 months of age, Staccato-like cough, rapid respiratory rate; NOTE: NO FEVER

71
Q

How is C. trachomatis pneumonia treated?

A

erythromycin

72
Q

How is C. trachomatis diagnosed?

A

minimal chest findings, xray hyperinflation and diffuse infiltrates, peripheral eosinophilia

73
Q

What is Legionella?

A

2-6% community acquired pneumonias; Gram negative bacilli- don’t stain with common reagents; Organisms contaminate water sources: air conditioning systems and water tanks

74
Q

Who are at risk for Legionella?

A

immunocompromised, hospitalized, and outbreak situations

75
Q

What is Legionella pathogenesis?

A

Aspiration or inhalation of organism; Flagellae and pili allow attachment to respiratory epithelium and macrophages

76
Q

What are the virulence factors for Legionella?

A

Exotoxins: (hemolysin, cytotoxin, deoxyribonuclease, ribonuclease) cause destruction by killing the infected respiratory cells leading to formation of microabscesses; Immunity primarily cell mediated immunity (T cells)

77
Q

What are the symptoms of Legionnaires disease?

A

influenza like illness or severe manifestation= pneumonia, Fever (105), rigors, cough, headache; Multilobular infiltrates and microabscesses; Extrapulmonary manifestations: CNS, diarrhea, abdominal pain, nausea; high mortality

78
Q

What is the serology for Legionnaires?

A

Serology >1:128 positive however late development of antibodies; Culture on special media

79
Q

How is Legionnaires treated?

A

macrolide or levofloxacin

80
Q

What is Bordetella pertussis?

A

Fastidious, gram negative coccobacilii; Spread by respiratory droplets; No bacteremia; Toxins cause local tissue damage (A-B toxin)

81
Q

How is pertussis confirmed?

A

culture and/or PCR

82
Q

How is pertussis treated?

A

Erythromycin or azithromycin (better tolerated, shorter course); VACCINATE!

83
Q

What is distinctive about TB bacillus?

A

cell wall is made of lipids, VERY slow growing - long period of treatment

84
Q

How is TB spread?

A

Entry portal is the lungs - spread by inhalation of droplet

85
Q

What happens in the Primary TB infection?

A

TB reaches alveoli; Replicates intracellularly within alveolar macrophages; Prevents acidification of phagosome w/in macrophage; Lack of immediate host immune response

86
Q

How does the body fight TB?

A

CD4 to alveolar macrophage; Proliferation of CD4; Release of IFNg; additional macrophage phagocytosis; TNFa released; granuloma formed - all of this is a problem if you are on TNF inhibitor!

87
Q

What happens after immune response to TB?

A

Patient asymptomatic or mild viral like syndrome in 85% of cases; Enlargement of hilar and peribronchial lymph nodes; Ghon complex with fibrosis and calcification of hilar nodes; Development of positive PPD

88
Q

Who is at risk for developing cavitary active TB?

A

Adolescents! Weird…

89
Q

What is tuberculosis pleurisy?

A

HYPERSENSITIVITY REACTION TO SMALL # OF ORGANISMS REACHING PLEURA IN PRIMARY INFECTION; EXUDATIVE PLEURAL EFFUSION; CULTURE NEGATIVE

90
Q

Where can TB hang out?

A

Lymph nodes (formation of scrofula); bones; renal TB - asymptomatic until calyx/pelvis ulcerated

91
Q

What happens in active TB?

A

Caseating necrosis, liquefaction, drainage into the bronchial tree; Cavity formation

92
Q

What kind of TB is most contagious?

A

Cavitary disease

93
Q

What are active TB symptoms?

A

Systemic symptoms non-specific: fever, fatigue, night sweats, weight loss; Pulmonary symptoms: cough, productive or dry; Hemoptysis - coughing up blood - (can be emergency symptom)

94
Q

How is TB diagnosed?

A

Sputum smear (but negative in 50% of non-cavitary); Sputum culture = gold standard (takes 2-6 wks); broth media

95
Q

What are keys to TB treatment?

A

Directly Observed Therapy; always use at least 2 drugs (start w/ 4 pending sensitivities); 6-9 months of treatment

96
Q

What is the first line drug for TB?

A

Isoniazid (INH) - bacteriocidal, good CNS coverage, can be used during pregnancy; passes through placenta and into breast milk

97
Q

What does INH do?

A

Inhibits synthesis of mycolic acid, a major component of bacterial cell wall

98
Q

What toxicity can INH cause?

A

Hepatitis, neuropathy

99
Q

What does Rifampin do for TB?

A

Bacteriocidal, shortens treatment length (6-9 months w/, 18-24 w/out); can be used in pregnancy, good CNS coverage

100
Q

How does Rifampin work?

A

Inhibits DNA-dependent RNA polymerase in susceptible strains of bacteria

101
Q

What are side effects of Rifampin?

A

GI upset, Can cause cholestatic jaundice, Skin rash, Thrombocytopenia (rare); major drug-drug reaction

102
Q

What’s the super weird thing about Rifampin?

A

Turns pee orange!

103
Q

What is the drug-drug reaction of Rifampin?

A

Induces CYP450 - affects protease inhibitors (used in HIV)

104
Q

What does Pyrazinamide (PZA) do for TB?

A

Main role in sensitive disease is to reduce length of treatment from 9 months to 6 months; NOTE: do not use in pregnancy

105
Q

What are the side effects of PZA?

A

Hyperuricemia - may cause gout (in which case STOP), hepatic toxicity

106
Q

What does Ethambutol (ETB) do in TB?

A

Prevention of resistance

107
Q

What is the toxicity associated w/ ETB?

A

Retrobulbar neuritis - red-green color blindness, blurred vision; do regular vision checks

108
Q

What is New Delhi Metallo-Beta Lactamase-1 (NDM-1)?

A

a transmissible genetic element (plasmid with integrons) encoding multiple antibiotic resistance genes including carbapenems, beta-lactams, macrolides, quinolones, rifampin - and spreading to lots of different bacteria!

109
Q

What is the key example of cross-resistance?

A

Methicillin resistance confers resistance to all beta-lactams, penicillins and cephalosporins (PBP-2a)

110
Q

What can be causes of cross-resistance?

A

Drug efflux pumps or overlapping targets

111
Q

Why is transfer of efflux pump resistance not easy to do?

A

complex genetic machinery needed for the pump to be functional

112
Q

Which antibiotics are routinely used in animal feed?

A

Macrolides, tetracyclines, glycopeptides

113
Q

How can we control the spread of antimicrobial resistance?

A
  1. Eliminate the use of antimicrobials in animal feed; 2. Restrict use of antibiotics for inappropriate indications; 3. Antibiotic restriction in hospital settings; 4. Enforce infection control policies; 5. tax antibiotics?

Infectious Disease 1 (10 decks)

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