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Infectious Disease & Public Health > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Which IFNs function in viral infection?

A
  • IFN alpha/beta (aka type I IFN)
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2
Q

How does innate immunity help combat viruses?

A
  • IFN alpha and beta (collectively known as type I IFN), NK cells, macrophages
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3
Q

How are IFNs released with viral infection? What are their functions? MOA?

A
  • Most viruses stimulate production of IFNalpha, beta (aka type I) when in cell
  • Function: inhibit viral replication in surrounding uninfected! host cells, increase MHC I, activate DCs and macrophages, activate NK cells
  • MOA: bind – activation of oligoadenylate synthetase and dsRNA-dependent protein kinase – activation of RNASE L and eIF2 alpha phosphorylated respectively – degrades mRNA and makes eIF2 inactive
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4
Q

Function of NK cells in virus infection? How?

A
  • Kill virus-infected cells early in infection (see how in another flash card)
  • How:
  • A. Mediate ADCC (antibody-dependent cell-mediated cytotoxicity): ab binds to cell, NK cells come along with FC receptor to ab, activated NK, apoptosis
  • B. Perforin-mediated osmotic death: many viruses reduce production of class I MHC to avoid CTL-induced lysis. Absence of MHC I removes NK cells from inhibitory state leading to infected cell death.
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5
Q

What chemical mediators produced by macrophages have anti-viral effects? How?

A
  • TNF-alpha and NO. These interfere with virus replication.
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6
Q

Which viruses infect macrophages? How can this be bad?

A
  • CMV, Ebola, HIV, measles, rubella

- Macrophages can traffic virus to many body sites.

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7
Q

Virus infections at mucosal sites vs systemic infections. Which leads to short-lived protective immunity? Long-lived?

A
  • Mucosal sites = short-lived

- Systemic = long-lived

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8
Q

Which arm of adaptive immunity is most important in early viral infections? During established viral infections?

A
  • Early = Humoral

- Established = Cell-mediated (CD8 CTLs)

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9
Q

Functions of ab in viral infection

A
  • Prevent virus from binding to target host cell
  • Opsonize virus to enhance phagocytosis
  • Activate complement to lyse viral envelopes
  • Facilitate ADCC by NK cells to lyse infected host cells
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10
Q

Functions of CD8 CTLs in viral infection

A
  • Produce TNF-alpha to interfere with viral replication

- Kill virally-infected cells via apoptosis and perforin-mediated mechanisms. Use of MHC I.

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11
Q

Order the following features of the immune system as response to viral infection
a. NK-mediated killing of infected cells

b. T-cell mediated killing of infected cells
c. Production of IFN-alpha, IFN-beta, TNF-alpha and IL-12

A
  • Order = C, A, B
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12
Q

Describe how memory T and B cells are different

A
  • Memory T cells = quiescent until reactivated by ag

- Memory B cells = actively producing serum ab for decades potentially

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13
Q

How to viruses attempt to evade the immune system?

A
  • Alter ags through point mutations or reassortment of genomes
  • Prevent class I MCH expression of viral peptides
  • Infection/killing of immune cells (eg. HIV and CD4+ T cells)
  • Latent infection
  • Infection of immunologically privileged site
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14
Q

Describe the deleterious effects of the immune response in viral infections

A
  • CTLs induce destruction of tissue (eg. hep B liver destruction)
  • Immune complex leads to kidney and arteriole destruction
  • Molecular mimicry: viral proteins are homologous with host normal tissue and immune system targets host
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15
Q

Examples of intracellular bacteria

A
  • Listeria monocytogenes, mycobacterium leprae, chlamydia trachomatis
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16
Q

What innate immunity mechanism acts to defeat intracellular bacterium?

A
  • Macrophages produce IL-12, which activates NK cells. NK cells produce IFN-gamma, which activates macrophages, leading them to become more efficient killers. Specifically, IFN-gamma leads to production of NO leading to some killing of intracellular bacteria.
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17
Q

What type of adaptive immune response deals with intracellular bacterium?

A
  • Delayed-type hypersensitivity (type 4) rxn.
  • T-cells are activated, secrete IFN-gamma, macrophages are activated.
  • IL-12 released by macrophages steering a TH-1 mediated response (cell-mediated). This leads to granuloma formation.
  • Granulomas impair replication: macrophages produce NO, fibrosis and calcification decreases nutrient and o2 supply.
  • Note: CTLs can be generated against bacteria that escape phagosomes intracellularly and have peptides presented on class I MHC.
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18
Q

How do intracellular bacteria evade the immune system?

A
  • Inhibition of fusion of phagosomes and lysosomes
  • Scavenging of ROS intermediates
  • Disruption of phagosome, escape into cytosol
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19
Q

What are the deleterious effects of the immune system in intracellular bacterial infections?

A
  • Granuloma formation can lead to severe compromise of normal tissue function.
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20
Q

In leprosy, which response leads to worse disease?

A
  • Tuberculoid: TH-1 mediated = milder dz (granuloma + few bacilli). Normal T cell response.
  • Lepromatous: TH-2 mediated = worse disease (many bacilli in lesions). Hypergammaglobulinemia.
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21
Q

Is the leading cause of acute otitis media viral, bacterial or fungal? Clinical implication of this?

A
  • Viral (70%). Wait 48 hrs to initiate tx.
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22
Q

Strep pneumo. Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in chains
  • Features: catalase neg, alpha hemolytic (green: partial), optochin sensitive, bile soluble, capsule +ve quellung test
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23
Q

How can staph and strep be differentiated by lab test?

A
  • Staph = catalase pos

- Strep = catalase neg

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24
Q

Staph aureus. Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in clusters
  • Features: catalase pos, coagulase pos
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25
Q

Staph epidermidis. Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in clusters
  • Features: catalase pos, coagulase neg, novobiocin sensitive
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26
Q

How can staph aureus be differentiated from other species?

A
  • S. aureus = coagulase pos, others = neg
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27
Q

Staph saprophyticus. Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in clusters
  • Features: catalase pos, coagulase neg, novobiocin resistant
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28
Q

Gram pos rods

A
  • Clostridium, corynebacterium, listeria, bacillus
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29
Q

Strep mutans (viridans strep). Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in chains
  • Features: catalase neg, alpha hemolytic (green: partial), optochin resistant, not bile soluble, capsule –ve quellung test
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30
Q

Strep pyogenes (Group A). Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in chains
  • Features: catalase neg, beta hemolytic (clear: complete), bacitracin sensitive
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31
Q

Strep agalactiae (Group B). Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in chains
  • Features: catalase neg, beta hemolytic (clear: complete), bacitracin resistant
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32
Q

Enterococcus faecalis. Gram stain, shape, lab/physiologic features?

A
  • G stain: pos
  • Shape: cocci in chains
  • Features: catalase neg, no hemolysis (gamma: none) *graph notes can also be alpha
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33
Q

Initial tx choice for acute otitis media? Recurrent or unresponsive OM? Otitis media with effusion/serous otitis media?

A
  • Acute otitis media: Amoxicillin. If contraindicated: TMP-SMX, azithro, cefuroxime
  • Recurrent or unresponsive: amoxicillin-clavulanate
  • Otitis media with effusion (sign of Eustachian tube dysfunction diagnosed with pneumotoscopy without infected fluid): watchful waiting (3 month minimum), refer to hearing/speech for TM tubes
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34
Q

Complications of otitis media

A
  • Perforation of TM, tympanosclerosis, cholesteatoma, mastoiditis, lateral sinus thrombosis, meningitis/brain abscess
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35
Q

Tx of otitis externa if fungal, bacterial, chronic/recurrent Swimmer’s ear?

A
  • Fungal: azole
  • Bacterial: neomycin/polymyxinB/hydrocortisone. If concerned about tissue penetration, tx with oral cipro
  • Chronic/recurrent Swimmer’s ear: 50:50 mix of isopropyl etoh and white vinegar. This dries out ear.
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36
Q

Typical tx of acute bacterial sinusitis

A
  • Amoxicillin, decongestants (not antihistamines as secretions are prevented from flowing and make illness worse), mucolytics
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37
Q

Complications of sinusitis

A
  • Meningitis, cavernous sinus thrombosis, boney invasion of the orbit
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38
Q

Tx of pseudomonas aeruginosa sinusitis

A
  • Hospitalization and IV fluoroquinolones
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39
Q

How is strep throat diagnosed?

A
  • Rapid strep test or throat culture (Gold standard)
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40
Q

Why is strep throat treated?

A
  • Prevent rheumatic cardiac disease, tx fever, symptom relief. Note: no reduction in formation of post-strep glomerulonephritis (immune complex dz)
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41
Q

Tx of strep throat

A
  • Penicillin

- Alternative: cephalexin, erythromycin, azithromycin

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42
Q

Complications of GAS infections

A
  • Peritonsilar abscess, retropharyngeal abscess, sepsis, rheumatic fever, post-strep glomerulonephritis, pneumonia
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43
Q

Signs/sx of post-strep glomerulonephritis

A
  • Hematuria, pyuria, RBC casts, edema, HTN, oliguric renal failure
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44
Q

Typical tx of Salmonella diarrhea

A
  • Supportive w/hydration, anti-diarrheal not indicated, abx NOT indicated (prolongs fecal shedding)
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45
Q

Neisseria meningitidis. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: cocci
  • Features: maltose fermenter
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46
Q

Neisseria gonorrhoeae. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: cocci
  • Features: maltose non-fermenter
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47
Q

Haemophilus influenzae. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: coccoid rods
  • Features: requires factors V (NAD) and X (hemin) for growth
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48
Q

Pasteurella. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: coccoid rods
  • Features: not specified
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49
Q

Brucella. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: coccoid rods
  • Features: not specified
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50
Q

Bordatella pertussis. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: coccoid rods
  • Features: not specified
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51
Q

Klebsiella. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: fast lactose fermenter
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52
Q

E.coli. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: fast lactose fermenter
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53
Q

Enterobacter. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: fast lactose fermenter
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54
Q

Citrobacter. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: slow lactose fermenter
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55
Q

Serratia. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: slow lactose fermenter
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56
Q

Shigella. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: lactose non-fermenter, oxidase neg
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57
Q

Salmonella. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: lactose non-fermenter, oxidase neg
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58
Q

Proteus. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: lactose non-fermenter, oxidase neg
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59
Q

Pseudomonas. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: lactose non-fermenter, oxidase pos
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60
Q

Gram neg rods that cause diarrhea. Which accompany fever? Watery diarrhea? Bloody?

A
  • ETEC, vibrio cholerae, salmonella, shigella, campylobacter jejuni, EPEC, EHEC (O157:H7)
  • No fever: ETEC, vibrio cholerae
  • Watery diarrhea: ETEC, vibrio cholerae, EPEC
  • Bloody diarrhea: EHEC, campylobacter jejuni
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61
Q

Which are the curved gram neg rods that cause diarrhea? Is it through invasion or toxin?

A
  • Campylobacter: inflammatory

- Vibrio cholerae: toxin

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62
Q

Which organisms cause diarrhea/food poisoning d/t pre-formed toxin?

A
  • Bacillus cereus, C. botulinum, C.perfringens, S.aureus
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63
Q

Which parasite causes bloody diarrhea? Profuse/voluminous watery? Fatty/foul-smelling?

A
  • Bloody: Entamoeba histolytica
  • Profuse/voluminous: cryptosporidium, cyclospora, isospora
  • Fatty/foul-smelling: Giardia
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64
Q

Tx for RSV

A
  • Watchful waiting. If underlying chronic condition with time in NICU, give ribavirin
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65
Q

Common agents responsible for aspiration pneumonia

A
  • Strep pneumoniae, Klebsiella pneumoniae, E.coli
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66
Q

Which genital lesions are painful? Painless?

A
  • Painful: chancroid (Haemophilus ducreyi), herpes

- Painless: syphilis (Treponema pallidum), penile carcinoma, granuloma inguinale, lymphogranuloma venereum

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67
Q

Cytological changes with herpes infection

A
  • Tzanck smear: large multinucleated cells
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68
Q

Haemophilis ducreyi. Gram stain, shape, lab/physiologic features?

A
  • G stain: neg
  • Shape: rods
  • Features: not specified
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69
Q

Tx for Haemophilis ducreyi chancroid

A
  • Azithromycin, ceftriaxone, cipro, erythromycin
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70
Q

Complications of chancroid

A
  • Inguinal adenitis, inguinal buboes-abscess and fistula formation, auto-inoculation, phimosis from scarring
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71
Q

Imaging modalities which allow for differentiation of cellulitis from osteomyelitis

A
  • X-ray. Osteomyelitis shows lytic lesions.
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72
Q

Bacterial agents responsible for causing cellulitis

A
  • staph aureus, staph epidermidis, pseudomonas, strep pyogenes
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73
Q

Tx of osteomyelitis

A
  • Surgical drainage/debridement, abx for weeks, control of BGL
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74
Q

2 great triumphs in public health

A
  • ID control (Smallpox eradication (35th anniversary), polio near control, vaccines) lengthening of quality of life (doubled in last century), safe drinking water, sanitation, MV safety etc.
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75
Q

Who are local public health authorities?

A
  • IDPH, PCHD (Polk county health department)

- CDC feeds data to regional and local systems

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76
Q

Who do you contact re: rabies advice, dosing etc.?

A
  • Animal control through police dispatch
77
Q

What local public health services are available?

A
  • Rabies, STD clinic, secure water, sanitary sewer, immunization clinics/travel advice
78
Q

Compare and contrast: quarantine to isolation

A
  • Quarantine: exposure to disease

- Isolation: suspected of having disease

79
Q

Which are reportable diseases?

A
  • Viral hemorrhagic fevers, TB, SARS, measles, cholera, diphtheria, meningitis, botulism, polio, plague, smallpox (eradicated)
80
Q

Does HIPAA apply to public health?

A
  • No, specifically does not.
81
Q

Current method of tracking births/deaths

A
  • Electronic paper
82
Q

Primary tools in public health

A
  • Analysis, action
83
Q

Greatest threat in public health

A
  • Return of ID
84
Q

Mechanisms by which extracellular bacteria cause destruction of tissue?

A
  • Induction of inflammation

- Toxins that kill host cells

85
Q

First line of defense against extracellular bacteria?

A
  • Phagocytosis via neutrophils (blood) and macrophages (tissue). Note: if asked on boards/exam which cell type arrives first, say neutrophils (marines).
86
Q

How do phagocytes recognize bacteria?

A
  • Polysaccharides, peptides (with RGD: arg-gly-asp). Also, they express Fc receptors and C3b receptors for IgG and C3b. Unmethylated CpG dinucleotide motifs activate macrophages too. IFN-gamma = most potent activator of macrophages.
  • Receptors that mediate this on phagocyte = Fc receptors, complement receptors, scavenger receptors, other integrins, lectins, TLRs (toll-like)
87
Q

How are iron concentrations lowered with bacterial infections?

A
  • Neutrophils release lactoferrin
88
Q

Effect of histamine in bacterial infections

A
  • Released from mast cells, enhances inflammatory process (upregulates binding proteins on ECs to aid extravasation)
89
Q

How is alternative complement pathway activated? Function of pathway?

A
  • Microbial surface (specifically peptidoglycan and LPS). Note: classic pathway requires ab binding.
  • Function = lyse gram neg (thin) via MAC, opsonize gram pos (thick) via phagocytes
90
Q

Deficiencies in C5-C9 lead to what infections?

A
  • Neisseria meningitidis infections
91
Q

What is the principle adaptive immune response against extracellular bacteria? How?

A
  • Humoral immunity
  • IgG: opsonizes and enhances phagocytosis
  • Toxin-specific abs: neutralize toxins
  • IgM and IgG: activate classical pathway of complement leading to bacterial lysis
92
Q

Why are neonates predisposed to infections between 3 and 6 months of age? What bacterial infections are they at risk for?

A
  • Maternal abs disappear

- Infections: Strep pneumo, N.meningitidis, H. influenza type B

93
Q

After infection with S. pyogenes and/or S. pneumo, why is one susceptible to these again?

A
  • Have many forms of M protein + polysacc capsule. Abs to one don’t confer protection against another.
94
Q

Function of IgA

A
  • Functions at mucosal sites:
  • Aggregates bacteria to facilitate expulsion
  • Prevents invasion of bacteria through the mucosal epithelium
  • Fixes complement
95
Q

In individuals with IgA deficiency, another Ig can compensate. Which one?

96
Q

How can extracellular bacteria attempt to evade the immune system?

A
  • Polysaccharide capsules: resist phagocytosis and inhibit complement activation via alternative pathway
  • Variation of surface antigens
  • IgA1 protease (eg. Neisseria and Haemophilus) to hamper mucosal immunity. Body produces IgA2.
  • Interfere with complement activation
  • Type III secretion system (S. typhi specifically): syringe of proteases to inhibit NFkB signaling and secretion of TNF-alpha
97
Q

What are the deleterious effects of the immune system during an extracellular bacterial infection?

A
  • Septic shock (hypotension + DIC): d/t many gram neg (LPS) and some gram pos which induce macrophages to release TNF-alpha and IL-1
  • Septic-shock-like rxn: superantigens bind class II MHC activating T cells producing TNF-alpha
  • Rheumatic fever: cross-reactive antibodies induced by strep M protein bind to sarcolemma proteins in heart leading to carditis
  • Post-strep glomerulonephritis: abs form complexes with ag that lodge in kidneys (type 3 hypersensitivity)
98
Q

Spirochetes

A
  • Treponema pallidum, borrelia burgdorferi, leptospira
99
Q

How is one infected with spirochetes?

A
  • Breaks in skin or via arthropod vectors
100
Q

Describe innate immune response against spirochetes

A
  • Not very good
  • Neutrophils: phagocytosis + killing. Cannot prevent dissemination though.
  • Alternative complement activated by Treponema, but not readily killed.
101
Q

Describe adaptive immune response against spirochetes

A
  • TH1 (cell-mediated) most effective against clearing organisms. IFN-gamma activates macrophages for better killing.
  • Ab helpful after latent syphilis
  • Classical complement activation critical for eradication of B.burgdorferi.
102
Q

How does T. pallidum evade the immune system?`

A
  • Lacks virulence factors. Resistant to normal host immune mechanisms.
103
Q

How does B. burgdorferi evade the immune system?

A
  • Coats itself with amorphous material to prevent phagocytosis + complement-mediated lysis. Evades adaptive immunity. So highly effective that nearly all exposed to this organism are productively infected.
104
Q

Deleterious effects of immune response seen in spirochete infections

A
  • Secondary syphilis: immune complexes (type 3) have role

- Likely T cells responsible for inducing Lyme arthritis

105
Q

Which cell type is highly effective in innate immunity against fungal infections?

A
  • Neutrophils (lesser degree macrophages). Neutropenic individuals highly susceptible to opportunistic fungal infections, esp. C. albicans.
106
Q

What is the dominant protective mechanism against disseminated candidiasis?

A
  • Innate immunity via neutrophils. This is unlike other fungal pathogens.
107
Q

What adaptive immune response is most important in combatting most fungal infections? Exception?

A
  • TH-1 (CMI). C. neoformans eliminated by CTLs. H.capsulatum housed away by granulomas.
  • Exception: C. albicans. Higher ab titers correlated with improved clinical outcomes.
108
Q

Which is most effective against parasitic infections – innate or adaptive immunity? Why?

A
  • Adaptive
  • Macrophages can phagocytize protozoa, but many resistant to killing.
  • Helminths have outer layer that activates complement, but resistant to killing. Also resistant to granules of neutrophils and macrophages.
109
Q

Function of IgE in parasitic infections?

A
  • Mast cells release histamines, which increases flow of lymph flushing ag into lymph nodes.
  • Also triggers muscular contraction to expel pathogens from gut
110
Q

What type of adaptive response is seen in parasitic infections – TH1 or 2?

A
  • Either. Once one response is in play, the other is downgraded.
  • TH1: CMI via CTLs, macrophage-mediated killing and/or IgG
  • TH2: IgE and infiltration by eosinophils
111
Q

How are protozoal (Leishmania and T. cruzi) infections combatted by the immune system?

A
  • They survive within macrophages. Macrophages stimulate TH1.
  • CD4 secrete IFN-gamma. NO produced by macrophages and they become more efficient at killing intracellular parasites.
  • IFN-gamma can also aid by depleting intracellular tryptophan which is essential for life by some parasites.
112
Q

How are schistosoma infections combatted by the immune system?

A
  • CD4 T cells recruit macrophages to form granulomas
113
Q

How are plasmodium infections combatted by the immune system?

A
  • TH1 mediated. CTLs are effective against intrahepatic stage. Abs produced against sporozoite and erythrocytic stages, but not effective as CTLs.
114
Q

How are helminthic infections combatted by immune system?

A
  • IgE. Used by eosinophils for ADCC.

- Note: clinical relevance – eosinophilia + elevated IgE = worm infection

115
Q

Strategies used by parasites to evade immune system

A
  • Concealed in intestinal lumen or forms protective cyst
  • Coats self with host protein
  • Outer surface inhibits complement, repairs damage
  • Enzymes that cleave membrane bound antibody
  • Surface antigen variation (trypanosomes)
  • Shed antigens
  • Suppression of macrophage IL-12 (needed for TH1 response)
116
Q

Describe deleterious effects of the immune response seen in parasitic infections

A
  • Dysregulated TH1 response = increased TNF-alpha production (highly prognostic of death)
  • Immune complex vasculitis and nephritis
  • Fibrosis and granuloma (in liver with Schistosoma)
  • Lodging in lymphatic channels = lymphedema (filariasis)
  • Chronic infections that induce strong TH2 inhibit TH1 immunity to vaccine antigens
117
Q

Most common pathogens associated with esophagitis

A
  • Candida albicans (most common): patchy non-ulcerative plaques!
  • Also HSV I > HSV II: ulcerations!. Microscopy shows inclusion.
  • CMV: ulcerations
118
Q

Sx/signs of esophagitis

A
  • Sx: Dysphagia with or without odynophagia, retrosternal pain
  • Imaging: cobblestoning, EGD: ulcers, non-ulcerative plaques
119
Q

Tx of esophagitis if candida, HSV or CMV

A
  1. Candida: oral fluconazole (preferred), IV echinocandin (-fungin endings) or amphotericin B
  2. HSV: acyclovir
  3. CMV: IV ganciclovir, oral valganciclovir
120
Q

Typical pathogens associated with stomach infections

121
Q

How is H.pylori infection diagnosed?

A
  1. Non-invasive studies: urea breath test, stool antigen test, serology not reliable for current infection
  2. Invasive studies: endoscopy urease, histology
122
Q

Tx for H.pylori infections

A
  • Previous: PPI+clarithromycin+amoxicillin
  • Now: rabeprazole+amox x 5; then rabeprazole+clarithro+tinidazole for another 5
  • Alternative: pepto+ticarcillin+metro+omeprazole
123
Q

Do H.pylori infections need test to see if cured?

A
  • Yes. Non-invasive tests preferred.
124
Q

Signs/symptoms that indicates diagnostic evaluation for GI tract infection

A
  • Profuse watery diarrhea w/signs of hypovolemia, passage of many small volume stools containing blood/mucus, bloody diarrhea, temp > 101.3 (38.5), passage of >=6 unformed stools/24 hrs of duration of illness > 48 hrs, severe abdominal pain, hospitalized patients or recent use of abx, diarrhea in elderly or immunocompromised, systemic illness w/diarrhea, community outbreaks
125
Q

Define diarrhea

A
  • 3 or more watery stools over a 24 hour period

- Acute 4 wks

126
Q

Typical pathogens associated with small/large intestine infections

A
  • C.diff, E.coli, salmonella, shighella
127
Q

What exposures are associated with C.perfringens?

A
  • Home-canned foods
128
Q

What exposures are associated with B.cereus?

A
  • Fried rice
129
Q

What exposures are associated with ETEC?

A
  • Travelers to developing world
130
Q

What exposures are associated with Salmonella?

A
  • Eggs (Caesar salad)
131
Q

What exposures are associated with C.diff?

A
  • Hospitalization, abx, chemo
132
Q

What exposures are associated with Listeria?

A
  • Dairy, pregnancy, neonates, immunocompromised
133
Q

What exposures are associated with Rotavirus?

A
  • Daycare, nurseries
134
Q

What exposures are associated with Norovirus?

A
  • Cruise ships, schools, nursing homes
135
Q

What exposures are associated with Hep A?

A
  • Overcrowding, lack of clean water, MSM
136
Q

What exposures are associated with CMV?

A
  • AIDs, organ transplantation
137
Q

What exposures are associated with Giardia?

A
  • Streamwater/spring water ingestion
138
Q

What exposures are associated with Entamoeba?

A
  • Mexico, MSM
139
Q

What exposures are associated with Cryptosporidium?

A
  • Swimming pools/parks
140
Q

What exposures are associated with Cyclospora?

A
  • Raspberries from Guatemala
141
Q

Non-inflammatory diarrhea.
a. Clinical presentation

b. Lab findings
c. Typical pathogens
d. Pathophysiology
e. Tx approach

A

a. Large volumes of watery stools, signs and sx of dehydration
b. Fecal leuk neg, acidosis, azotemia (high levels of nitrogen)
c. Vibrio cholerae, ETEC
d. Toxin-mediated secretory diarrhea
e. Rehydration and abx

142
Q

Inflammatory diarrhea
a. Clinical presentation

b. Lab findings
c. Typical pathogens
d. Pathophysiology
e. Tx approach

A

a. Dysentery: small quantities of blood, mucous, often with fever!
b. Fecal leuk pos
c. Shigella, Salmonella, Campylobacter jejuni
d. Compromise of intestinal epithelium with varying invasion
e. Abx if severely ill or immunocompromised

143
Q

Hemorrhagic diarrhea
a. Clinical presentation

b. Lab findings
c. Typical pathogens
d. Pathophysiology
e. Tx approach

A

a. Grossly blood BM
b. Anemia, azotemia in setting of HUS
c. EHEC (O157:H7)
d. Poorly understood
e. Supportive. Don’t tx with abx! This may precipitate or increase risk for HUS.

144
Q

Diagnosis of C.diff

A
  • Pos stool test for C.diff toxins A or B (cell cytotoxin assay or PCR toxin gene detection – this is test of choice)
  • OR direct visualization of pseudomembranes in gut (100% specific)
145
Q

Clinical presentation of C.diff

A
  • Mild to moderate diarrhea, to fulminant and sometimes fatal pseudomembranous colitis
  • Hx of abx or chemo received within previous 8 weeks in most patients
146
Q

Tx for C.diff

A
  • Main three drugs: vancomycin, metronidazole, fidaxomicin.
  • Metronidazole for mild-moderate
  • Vanc (oral) for severe, complicated. High (500 mg QID) or low (125 mg QID) dose equally effective. Note VRE.
  • NB: no advantage to combo metronidazole plus rifampin
147
Q

Why be cautious with metronidazole in C.diff?

A
  • Can use it with first recurrence. Don’t use beyond first recurrence or for long term chronic therapy. Why? Can cause really painful peripheral neuropathy.
148
Q

Tx for lower GI infections

A
  • Supportive (fluids, electrolyte replacement)
  • Pepto or antiperistaltic agent if watery diarrhea without fever or blood in stool.
  • Pathogen specific abx when indicated.
149
Q

Sites of infection for UTI. Causes?

A
  1. Blood borne leading to renal parenchyma infection: TB, gram –ve sepsis.
  2. Ureter: obstruction, FB (stent)
  3. Uretero-vesicular junction
  4. Bladder: incomplete emptying, FB (cath, stent)
  5. Urethra: STD, FB
150
Q

Upper vs lower UTI

A
  • Upper: above vesicoureteral valves

- Lower: below vesicoureteral valves

151
Q

Complicated vs uncomplicated UTI

A
  • Complicated: tissue involvement, instruments, co-morbidities
  • Uncomplicated: local effects only or upper UTI without co-morbidities
152
Q

Pyelonephritis vs cystitis

A
  • Pyelonephritis: kidney, calyces, pelvis

- Cystitis: bladder

153
Q

Compare and contrast: recurrence vs relapse vs reinfection pertaining to UTI. Which has highest chance of resistance?

A
  • Recurrence: 3 or more UTIs/year
  • Relapse: recurrence in a month with same organism (ie. treatment failed)
  • Reinfection: relapse, but > 1 month, usually different organism. Highest chance of resistance.
154
Q

How do male/female UTI frequencies change between neonate to child-bearing years to middle/late adulthood

A
  • Neonate: males
  • Child-bearing: females
  • Middle/late: males = females
155
Q

Risk factors for UTI

A
  • Prior hx, reflux (incompetence of bladder valve), uncircumsized, sexual intercourse, IgA deficiency?, obstruction (prostate enlargement, ureteral stones)
156
Q

When should asymptomatic UTIs be treated?

A
  • Pregnancy, renal transplant, before uro surgery. Commonly seen in nursing home residents – don’t treat or check.
157
Q

Most common pathogens associated with UTIs

A
  • E.coli (80%), Staph saprophyticus (sexually active 15% of cases)
158
Q

What is the meaning of epithelial cells:WBC from UA?

A
  • If epi roughly = or higher than WBC, then contaminated with skin flora unless 0 of each. Cannot rely on results if contaminated.
159
Q

pH of urine dipstick with E.coli

A
  • pH below physiologic normal
160
Q

Meaning of specific gravity

A
  • Normal (equivalent to serum) = 1.010
  • Dehydration: > 1.010 (salt in excess to water)
  • Extra-hydrated:
161
Q

Check cases for L9

A

Check cases for L9

162
Q

Tx for GC/chlamydia

A
  • Ceftriaxone + Azithromycin
163
Q

Should catheters be placed in cases of pyelonephritis?

A
  • No. Don’t put FB into infected space.
164
Q

Describe tx for females of childbearing years with prior history of UTI and good followup with current UTI

A
  • Tx without testing
165
Q

What is complication of pyelonephritis with stone?

A
  • Intra-abdominal abscess
166
Q

Tx for cystitis

A
  • TMP/SMT for 3 days
167
Q

SIRS definition and criteria

A
  • Systemic inflammatory response syndrome
  • Criteria:
    1. Temp > 38 deg C (101.4 deg F) OR 90 bpm
    3. RR > 20 bpm or PaCO2 12K, 10%
168
Q

Sepsis definition

A
  • 2/4 SIRS criteria + infection (suspected or identification)
169
Q

Severe sepsis definition

A
  • = Sepsis + organ dysfunction

- = 2/4 SIRS criteria + infection + organ dysfunction

170
Q

Hemodynamic signs of organ dysfunction

A
  • Hemodynamic: SBP 40 OR
171
Q

Pulmonary signs of organ dysfunction

A
  • ALI w/PaO2/FiO2
172
Q

Hepatic signs of organ dysfunction

A
  • Bili > 4.0
173
Q

Renal signs of organ dysfunction

A
  • Cr > 2.0 (increase > 0.5)
174
Q

Hematologic signs of organ dysfunction

175
Q

Septic shock definition

A
  • Sepsis + hypotension despite 30ml/kg fluid resuscitation
176
Q

See cases L10

A

See cases L10

177
Q

Pathophysiology of sepsis

A
  • Activation of pro-inflammatory cytokines = reduction in SVR = hypotension = distributive shock = myocardial depression = BM suppression = activation of DIC = organ dysfunction
178
Q

Most common causes for sepsis. Most common pathogens?

A
  • UTIs, PNA and GI infections
  • pathogens: S.aureus and S. pneumoniae most common gram pos; E.coli, klebsiella and pseudomonas are predominant gram negs
179
Q

Clinical presentation of sepsis: ssx, PE

A
  • Non-specific: fever, chills, sweats, weakness, malaise, AMS, coagulopathy, report by patient of impending doom, pale/discolored, somnolent/sleepy, SOB
  • Source specific: skin, respiratory, GI, GU, blood-borne (non-specific)
  • PE: toxic appearance, discomfort, sweaty, cold, mottled skin, pallor, delayed cap refill, source specific findings (skin, hardware, CV, respiratory, abdominal, GU, CNS)
180
Q

Population at risk for sepsis

A
  • Chronic illnesses (DM), malnutrition, malignancy, immunosuppression, chronic use of steroids, immune deficiencies, post-transplant
181
Q

CBC findings in sepsis

A
  • CBC: leukocytosis or leukopenia; thrombocytosis or thrombocytopenia, anemia
182
Q

Labs to order in sepsis

A
  • Cr, K, bicarb, lactate, glycemia, LFTs, coagulation panel, ABG
183
Q

When should abx be initiated in sepsis?

A
  • After obtaining blood cultures. Within 1 hour of diagnosis. Give empiric combo therapy to cover all likely pathogens. Following BC results, de-escalate to targeted therapy based on sensitivities.
  • Note: BCs typically pos in only 1/3rd case
184
Q

Gold standard literature for management of severe sepsis and septic shock

A
  • Surviving sepsis campaign
185
Q

Goal MAP for sepsis mgmt.

186
Q

Describe fluid mgmt. in sepsis

A
  • Crystalloids = primary choice. Initial fluid of 30ml/kg.
187
Q

How would tx proceed if hydration wasn’t helping sepsis?

A
  • Pressors: NE best.
188
Q

Clinical signs of therapy adequacy in sepsis

A
  • *
    1. Downward trend of lactate
  1. MAP >= 65
  2. Venous separation >= 70%
  3. CVP: 8-12 mmHg
  4. UOP: > 0.5 ml/kg/hr

Infectious Disease & Public Health (2 decks)

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