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Infectious Disease & Public Health > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Compare and contrast the following: impetigo, folliculitis, furuncles/carbuncles, erysipelas, cellulitis, necrotizing cellulitis/fasciitis, chancriform/chronic nodular lesions

A
  • Impetigo: superficial skin infection
  • Folliculitis: infection in hair follicle
  • Furuncles/carbuncles: abscess(es)
  • Erysipelas (clear cut boundaries w/prominent edges): infection of dermal lymphatics/upper dermis
  • Cellulitis: infection of subq skin tissue
  • Necrotizing cellulitis/fasciitis: infection of deep skin fascia
  • Chancriform/chronic nodular lesions: ?
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2
Q

Microbial etiology of impetigo

A
  • Strep pyogenes, staph aureus
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3
Q

Most superficial skin and soft tissue infections are due to what microbe

A
  • Gram positive organisms unless exposure history suggests otherwise
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4
Q

Microbial etiology of erysipelas

A
  • Strep pyogenes
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5
Q

Microbial etiology of folliculitis and furuncle

A
  • Staph aureus
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6
Q

Microbial etiology of cellulitis

A
  • Strep pyogenes, staph aureus
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7
Q

Hot tub/whirlpool folliculitis microbe. Tx?

A
  • Pseudomonas aeruginosa

- Tx: resolves spontaneously in most cases, usually NO antimicrobial therapy needed

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8
Q

See L11 cases

A

See L11 cases

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9
Q

Tx of furuncle

A
  • I&D often sufficient. Give abx if cellulitis or co-morbidities
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10
Q

Tx of non-purulent cellulitis

A
  • 1st generation cephalosporin OR anti-staph penicillins (nafcillin, dicloxacillin)
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11
Q

Tx of purulent SSTI (skin and soft tissue infection)

A
  • These have possibility of being MRSA.
  • DRAINAGE
  • Vanc IV OR PO: TMP-Sulfa, clindamycin, minocycline
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12
Q

Microbial agents responsible for necrotizing cellulitis / fasciitis

A
  • C. perfringens (most common), Group A streptococci (strep pyogenes; flesh-eating), polymicrobial (gram neg rods + gram pos cocci), MRSA
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13
Q

Clinical features of necrotizing cellulitis/fasciitis

A
  • Severe constant pain (out of proportion to findings), bullous lesions, systemic toxicity (fever, toxic appearance, AMS), gas in soft tissues (per radiographs), rapid spread
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14
Q

Microbial etiology of chancriform/chronic nodular lesions

A
  • Sporothrix (Rose gardner’s dz, linear nodular lesions), mycobacterium marinum (swimming pool granuloma), bacillus anthracis (animal hide/skin), Francisella tularensis, other = nocardia, leishmania, blastomycosis
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15
Q

Route of spread for septic arthritis

A
  • Hematogenous = most common. Also direct inoculation, contiguous spread.
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16
Q

Risk factors for septic arthritis

A
  • RA, steroid use, DM
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17
Q

Most common microbial etiology of septic arthritis

A
  • Staphylococcus (staph aureus in most, if prosthetic joint = coag neg staph) = 70% of infections
  • Other = streptococci, gram neg, eikenella (human bite), pasteurella (cat bit), etc.
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18
Q

Clinical features of septic arthritis

A
  • Monoarticular (often knee), pain/swelling/redness/warmth, fever, tenderness
  • SSx subtle in immunocompromised or those with RA. Also indistinguishable from crystal arthritis, acute RA or hemarthrosis
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19
Q

Describe the synovial fluid in septic arthritis

A
  • Purulent, > 60K WBC
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20
Q

Risk factors for disseminated gonococcal infection

A
  • Sexually active, most cases ages
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21
Q

Tx for N.gonorrhoeae septic arthritis

A
  • 3rd Gen cephalosporin or fluoroquinolone
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22
Q

Tx for S. aureus septic arthritis

A
  • Nafcillin, 1st Gen cephalosporin or vanco
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23
Q

Tx for GAS septic arthritis

A
  • PCN or ceph
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24
Q

Tx for gram neg septic arthritis

A
  • Ceph, fluoroquinolone or carbapenems
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25
Q

Tx guidelines for septic arthritis

A
  • IV for 2-4 weeks
  • 2 weeks for gonococcal
  • 4 weeks for S.aureus and gram neg
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26
Q

Classification of osteomyelitis

A
  • Hematogenous (distant focus): per lecturer, think peds patient
  • Contiguous: per lecturer, think DM patient with lesion
  • Direct inoculation
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27
Q

In what situations/underlying risk factors is contiguous osteomyelitis seen?

A
  • Post-traumatic (open fx, surgery), peripheral neuropathy, vascular insufficiency, pressure ulcers. Lecturer emphasized diabetic patient with lesion.
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28
Q

Most common microbial etiology of osteomyelitis

A
  • > 50% of cases: staph aureus
  • Less common = coag-neg staph
  • Many other less common
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29
Q

How is osteomyelitis diagnosed?

A
  • Probe to bone (high predictive value in DM patients), MRI (best, std of care), bone biopsy
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30
Q

Puncture wound osteomyelitis

A
  • Pseudomonas aeruginosa
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31
Q

Tx of osteomyelitis

A
  • Abx

- Surgery (deep tissue sample or debridement)

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32
Q

What is considered lower respiratory tract?

A
  • Structures below pharynx
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33
Q

Broad-based budding yeast

A
  • Blastomycosis
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34
Q

Rusty sputum

A
  • Pneumococcal (strep pneumo)
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35
Q

Foul sputum

A
  • Lung abscess
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36
Q

Microbes associated with alcoholism that leads to RTI

A
  • Strep pneumo, oral anaerobes, Klebsiella, Acinetobacter, MTB
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37
Q

Microbes associated with COPD/smoking that leads to RTI

A
  • H. influenza, pseudomonas, legionella, Strep pneumo, Moraxella, Chlamyodphila pneumonia
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38
Q

Microbes associated with aspiration that leads to RTI

A
  • Gram neg enterics, oral anaerobes
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39
Q

Microbes associated with lung abscess that leads to RTI

A
  • MRSA, oral anaerobes, endemic fungal pneumonia, MTB, atypical mycobacteria
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40
Q

Microbes associated with bat/bird droppings that leads to RTI

A
  • H. capsulatum
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41
Q

Microbes associated with birds that leads to RTI

A
  • Chlamydophila psittaci
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42
Q

Microbes associated with rabbits that leads to RTI

A
  • Francisella tularensis
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43
Q

Microbes associated with farm animals/parturient cats that leads to RTI

A
  • Coxiella burnetii (Q fever)
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44
Q

Acid-fast bacilli microbes associated with respiratory tract infections

A
  • Mycobacteria or nocardia
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45
Q

Non-infectious etiologies of respiratory tract infections

A
  1. Neoplastic disorders: bronchogenic carcinoma, bronchioalveolar cell carcinoma, lymphoma
  2. Immunologic disorders: vasculitis, bronchiolitis obliterans, eosinophilic pneumonia, AIP, pulmonary alveolar proteinosis, sarcoidosis, SLE
  3. Drug toxicity
  4. Pulmonary vascular abnormalities: heart failure, PE
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46
Q

SSx of sinusitis

A
  • Nasal obstruction, focal facial pressure/pain, purulent nasal discharge, reduced smell
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47
Q

Testing for sinusitis

A
  • Nothing usually!
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48
Q

Most common causes of sinusitis

A
  • Viral infections, allergies
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49
Q

SSx of pharyngitis

A
  • Sore throat, dysphagia, URI symptoms, absence of cough, fever
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50
Q

Tests for strep throat

A
  • Rapid antigen, culture
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51
Q

Etiologies of pharyngitis and how to test

A
  • Strep: rapid antigen, culture
  • HIV: HIV ab, HIV RNA
  • EBV: monospot, EBV serologies, blood smear
  • Influenza: rapid test
  • Gonorrhea: throat culture
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52
Q

Typical cause of bronchitis

A
  • Usually viral: rhino, parainfluenza, influenza, corona, RSV, metapneumovirus
  • Others = B.pertussis, atypical bacteria
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53
Q

SSx of bronchitis

A
  • Cough predominant, fever
  • PE: +/- rhonchi
  • This is clinical diagnosis
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54
Q

Precautions for MRSA pneumonia

A
  • Contact precautions
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55
Q

What respiratory tract infections is drop precautions required?

A
  • Microbe > 5 microns

- Influenza, pertussis, adenovirus

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56
Q

What respiratory tract infections is airborne precautions required?

A
  • Microbe
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57
Q

L12 cases

A

L12 cases

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58
Q

Reservoir for HIV

A
  • Memory CD4 T cells
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59
Q

Definition of AIDS

A
  • CD4 T cells
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60
Q

Clinical relevance of viral load setpoint

A
  • Low = progression to AIDS delayed

- High = progression to AIDS accelerated

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61
Q

AIDS indicator diseases

A
  • Kaposi’s sarcoma
  • Dementia
  • Wasting
  • Pneumocystis
  • Toxoplasmosis
  • Cryptococcus
  • CMV
  • MAC
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62
Q

Non-AIDS Problems

A
  • Bacterial pneumonia, zoster, thrush, oral hairy leukoplakia, anemia, HPV-related dz, anemia, immune thrombocytopenia, neurosyphilis, LAD
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63
Q

HIV risk groups

A
  • MSM, heterosexual, IV drug users
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64
Q

Sx of acute HIV retroviral syndrome

A
  • Majority of cases: flu or mono syndrome

- Other sx: pharyngitis, rash, HA, aseptic meningitis, oral ulcers, genital ulcers

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65
Q

What is the earliest possible test to check for HIV-1?

A
  • Viral RNA (up to 3 weeks before HIV ab)
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66
Q

What HIV tests are available?

A
  • Viral RNA (up to 3 weeks before antibody)
  • HIV-1 p24 antigen (up to 1 week before antibody)
  • HIV antibody
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67
Q

Which HIV tests require confirmatory testing if positive?

A
  • Viral RNA and antigen/antibody tests

- Two-step testing (screening and confirmatory) is always necessary

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68
Q

Gold standard for HIV ab test

A
  • ELISA
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69
Q

What confirmatory tests are there for HIV?

A
  • HIV-1 western blot

- Multispot HIV-1/2 test

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70
Q

USPSTF screening recommendations for HIV testing

A
  • Screen persons ages 15 to 65 for HIV routinely. Grade A.
  • Not mandatory. Opt out testing.
  • Repeat based on risk. Pregnant women must be tested per Iowa law
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71
Q

Which HIV virus is less pathogenic?

A
  • HIV-2
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72
Q

Strains of HIV

A
  • R5-tropic: uses CD4 + CCR5 to gain entry into monocytes, macrophages and CD4 T cells
  • X4-tropic: uses CXCR4 + CD4 to gain access to T cells.
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73
Q

Which HIV strain is essential for transmission?

A
  • R5-tropic
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74
Q

Which HIV strain is associated with more rapid progression of HIV to AIDS?

A
  • X4-tropic
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75
Q

What mutation leads to no HIV infection?

A
  • Delta 32 CCR5 homozygosity mutation
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76
Q

What should be done to minimize the risk of mother to baby transmission?

A
  • Begin mom on HIV tx early in pregnancy, give baby post-exposure Prophy, don’t breast feed
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77
Q

Transmission of HIV from mother to baby typically occurs through what route?

A
  • Vaginal delivery (2/3)
  • In utero (1/3) later in gestation
  • Post-natally: breast feeding
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78
Q

When can secondary syphilis happen in HIV patients?

A
  • At any CD4 count
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79
Q

How much does life span decrease by with late HIV diagnosis?

A
  • 10-30 years
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80
Q

Most common AIDS-defining illness?

A
  • Pneumocystis jiroveci
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81
Q

At what CD4 count is PCP pneumonia seen?

A
  • CD4
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82
Q

Tx for pneumocystis pneumonia

A
  • TMP-SMX
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83
Q

At what CD4 count is MAC infection seen? Tx?

A
  • CD4
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84
Q

At what CD4 count is toxoplasma infection seen? Tx?

A
  • CD4
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85
Q

What opportunistic infections is primary prophylaxis given in AIDS patients?

A
  • Pneumocystis, toxoplasma, MAC
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86
Q

What opportunistic infections is secondary prophylaxis given in AIDS patients?

A
  • Pneumocystis (>200), toxoplasma (>200), MAC (>100), CMV, Cryptococcus, Histoplasma
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87
Q

Tx for HIV

A
  • Combination ART = 3 active drugs
  • Options are:
    1. Tenofovir + emtricitabine + efavirenz
    2. Teno + emtri + rilpivirine
    3. Teno + emtri + elvitegravir or cobicistat
    4. Abacavir + lamivudine + dolutegravir
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88
Q

Anti-retroviral drug classes

A
  1. CCR5 co-receptor antagonist *do tropism testing before placing on this medication
  2. Fusion inhibitor: binds gp41 * used in those who have failed everything else
  3. RTI (NRTI, NNRTI): inhibit reverse transcription
  4. INSTI (integrase strand transfer inhibitor): blocks integration
  5. Protease inhibitor (PI): blocks particle maturation
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89
Q

What is IRIS?

A
  • Atypical inflammatory disorders associated with immune recovery in HIV/AIDS patients
  • Typically have to give steroids, gets better
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90
Q

HIV Drug class with highest risk for drug-drug interaction

A
  • PI. Decreases effectiveness of BC pills
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91
Q

Which HIV drug class is teratogenic?

A
  • Efavirenz (NNRTI) – teratogenicity observed in monkeys
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92
Q

Which HIV drug requires HLA testing? Why?

A
  • Abacavir. Requires HLA-*B5701 testing. Risk for hypersensitivity with +ve HLA status.
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93
Q

Prior hx of AIDS increases risk for what co-morbidities?

A
  • Dyslipidemia, CV dz, squamous cell carcinoma of anus (without hx of anal intercourse), metabolic syndrome
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94
Q

Which viruses are members of human herpes virus family?

A
  • HSV-1, HSV-2, VZV, EBV, CMV

- Also HHV (6A, 6B, 7 & 8)

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95
Q

Common properties of human herpes viruses

A

a. Replicate in cell nucleus

b. Latency in host

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96
Q

Pathogenesis of herpes simplex virus

A
  • Exposure at mucosa/skin
  • Replication in sensory/autonomic nerves
  • Viral genome maintained in ganglion
  • Reactivation = at original site of infection
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97
Q

Transmission of HSV

A
  • Lesions or from asymptomatic excretion/shedding
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98
Q

Causes of reactivation of HSV

A
  • UV light, immunosuppression, trauma, sleep, stress
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99
Q

Tropism of HSV-1 & 2

A
  • HSV-1: oral mucosa (herpes labialis)
  • HSV-2: anogenital mucosa (herpes genitalis)
  • Can cause lesions at any location though
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100
Q

Compare and contrast clinical presentation of primary HSV infection to reactivation

A
  1. Primary: sudden, most asymptomatic in immunocompetent, lesions painful lasting up to 2 weeks
  2. Reactivation: rarely associated with systemic signs, can present with local LAD, prodrome (pain, burning, tingling, pruritus), lasts hours to 3 days
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101
Q

Clinical syndromes associated with HSV

A
  1. Oral-facial infections
  2. Genital infections
  3. Herpetic whitlow
  4. Herpes gladiatorum: common in wrestlers on forearms
  5. Herpetic eye infections: emergency leading to retinitis. Other eye conditions = necrotizing retinitis, HSV keratitis.
  6. CNS infection: encephalitis, aseptic meningitis, Mollaret syndrome, transverse myelitis, Bell’s palsy
  7. Visceral infections: esophagitis, tracheitis, HSV pneumonitis/hepatitis
  8. Immunocompromised: recurrent infections, disseminated
102
Q

Presentation of herpes simplex encephalitis?

A
  • Acute, sporadic encephalitis with fever and focal signs
  • Temporal lobe enhancement
  • Poor survival!
103
Q

What is Mollaret syndrome?

A
  • Occasionally recurrent meningitis associated with reactivation of HSV
104
Q

How is HSV diagnosed?

A
  • Clinically (painful vesicular lesion with surrounding erythematous base)
  • Tzanck smear: intranuclear inclusions. Cannot differentiate from VZV
  • Best = PCR.
  • Culture takes too long
  • Serology
105
Q

Tx of HSV infections

A
  • Acyclovir
  • Others = foscarnet, ganciclovir, famciclovir, valacyclovir. For eye infections, use topical agents occasionally with oral acyclovir.
106
Q

Agent responsibility for chickenpox and zoster

A
  • Primary infection with VZV = varicella (chickenpox)

- Reactivation with VZV in sensory dorsal root ganglia = zoster (aka shingles)

107
Q

Lesions characteristic of chickenpox

A
  • Lesions at different stages
108
Q

When is chickenpox contagious?

A
  • 48 hours before vesicles until crusting
109
Q

Transmission of chickenpox

A
  • Highly contagious

- Aerosolized droplets from nasopharynx or direct contact with vesicle fluid

110
Q

Clinical manifestations of VZV infection

A
  • Exanthem (widespread rash), enanthem (rash on mucous membranes), bacterial skin superinfections, visceral involvement (CNS, pneumonitis, hepatitis), disseminated (in immunocompromised)
111
Q

Most common visceral complication of VZV infection. Risk factors?

A
  • Pneumonia
  • High mortality
  • Risk factors: smoking, pregnancy, immunosuppression
112
Q

Tx of varicella

A
  • Acyclovir
113
Q

Who gets varicella vaccine?

A
  • Ongoing risk of exposure (daycare), household contacts of immunosuppressed pts, women of childbearing age, outbreaks with intense exposure, post-exposure Prophy in non-immune patients of children with chickenpox
114
Q

Most common sensory dorsal root ganglia where VZV reactivates?

A
  • T3-L3
115
Q

Clinical characteristics of shingles

A
  • Pain may precede lesions
  • Usually 1 dermatome is affected but can affect 2-3 (disseminated typically in immunocompromised)
  • Lesions at same stage
116
Q

Clinical manifestations of herpes zoster

A
  • Cutaneous, acute neuritis, PHN: post-herpetic neuralgia, ocular, oticus (ramsey-Hunt syndrome), CNS (aseptic meningitis, myelitis, encephalitis, stroke syndrome), pneumonitis, hepatitis
117
Q

How is zoster diagnosed?

A
  • Tzanck smear, culture, PCR, serology
118
Q

Tx of zoster

A
  • Acyclovir = best. Other = Valacyclovir, famciclovir, foscarnet. Prompt tx decreases incidence of prolonged PHN: post-herpetic neuralgia
  • VZIG (specific Ig)
  • Care for lesions. Avoid aspirin (d/t Reye syndrome).
119
Q

How is EBV different to other herpes viruses?

A
  • No cytopathic effect. Transforms host cells.
120
Q

Tropism of EBV

A
  • Lymphotropic (B and T cells), epithelial cells and myocytes
121
Q

Transmission of EBV

A
  • Saliva
122
Q

Clinical manifestations of EBV in adolescents/adults

A
  • Mononucleosis

- Fever, adenopathy, pharyngitis, splenomegaly, rash in 5% (if amp given, 90-100%)

123
Q

Tx of EBV mono

A
  • Most sxs resolve in 3 weeks
  • Supportive
  • Avoid contact sports for 6-8 weeks
  • Steroids if airway obstruction, aplastic anemia, fulminant hepatitis
124
Q

Complications of infectious mono

A
  • Hematologic
  • SPLENIC RUPTURE (2/1000)
  • Neurologic complications
  • Hepatic
  • Cardiac
  • Pulmonary
125
Q

EBV associated malignancies

A
  • Lymphoproliferative disorders (HLH: hemophagocytic lymphohistiocytosis, lymphomatoid granulomatosis)
  • Duncan syndrome
  • Burkitt’s lymphoma
  • Nasopharyngeal carcinoma
  • Hodgkin’s disease
  • T-cell lymphoma
  • Nasal lymphoma
126
Q

How is EBV infection diagnosed?

A
  • Clinical presentation

- Lab: heterophil abs, atypical lymphocytosis, EBV specific abs (VCA), PCR

127
Q

Differential for EBV infection

A
  • EBV, CMV, strep, CMV, rubella, mumps, hepatitis, toxoplasmosis, drug rxns, acute HIV
128
Q

Transmission of CMV

A
  • Childhood, sexual, transfusion/transplantation
129
Q

Histologic findings with CMV

A
  • Large cells with intranuclear owl eye inclusions. Occasionally cytoplasmic inclusions.
130
Q

Clinical manifestations of CMV

A
  1. CMV mononucleosis: esp in sexually active young adults
  2. Immunocompromised: complication of transplantation, hepatitis, pneumonia, esophagitis, gastritis, colitis, retinitis, GI CMV
  3. Congenital CMV
131
Q

Virus that complicates transplantation of organs

A
  • CMV
132
Q

Clinical presentation of CMV mono

A
  • Exudative pharyngitis and cervical adenopathy is rare opposed to EBV mono
  • Alk phos and transaminases usually elevated
  • Esp seen in sexually active young adults
133
Q

Clinical presentation of CMV complication post-transplantation

A
  • Fever 1-4 months post-op, leukopenia
134
Q

Diagnosis of CMV

A
  • PCR, serology
135
Q

Tx of CMV

A
  • Ganciclovir, valganciclovir, foscarnet
136
Q

Importance of administering immunizations according to the periodicity schedule

A
  • Ensures optimal individual immune response

- Ensure strong community immunity

137
Q

What is the first vaccine?

A
  • Hep B
138
Q

Risk vs benefit of

a. Hep B

A
  • Risks: soreness, temp of 99.9 or higher

- Benefits: in 2009 38K infected, each year about 2-4K die from cirrhosis or liver cancer d/t hepB

139
Q

Is there a way to give less shots?

A
  • Administer combo vaccines. Spreading shots out has no evidence.
140
Q

AAP statement on alternative immunization schedule

A
  • No alternative schedule. Delaying leaves a child at risk for a longer period of time and does not make vaccinating safer.
141
Q

When to delay/not give immunization?

A
  • A chronic health condition
  • A weakened immune system (chemo, certain meds after transplant)
  • Had a severe allergic rxn
142
Q

Does illness prevent immunization?

A
  • A child may be vaccinated if mild illness (low grade fever
143
Q

Risk vs benefit of

b. Varicella

A
  • Risks: mild rash up to 1 month, possible but rare to infect other members of household, fever, pain, swelling, rare: pneumonia, seizure
  • Benefits: before vaccine 12K hospitalized per year – pneumonia, bacterial infection, encephalitis; about 100 died/year, less severe dz if contracted with vaccine
144
Q

Risk vs benefit of

c. HPV

A
  • Risks: pain, redness, swelling, mild to moderate fever, headache
  • Benefits: protection against 9 serotypes, 12K women get cervical cancer or other genital cancers from HPV each year, head, neck and anal cancers in men 7K per year.
145
Q

What is the IRIS system?

A
  • Iowa’s immunization registry information system. IRIS provides instant access to patient’s immunization status and creates reminders/recall notices for immunizations etc.
146
Q

Define the AAP recommended response to caring for children with parents that refuse vaccination

A
  • Should not discharge patients
  • Listen to concerns
  • Discuss specific vaccines separately
  • Discuss strategies to limit pain
  • Ongoing relationship to discuss immunizations at subsequent visits
147
Q

Ways to decrease pain with immunization

A
  • Don’t aspirate
  • Inject most painful vaccine last
  • Breast/formula feed during vaccination OR give sugar solutions before
  • Hold child
  • Upright position for child > 3. Don’t restrain
  • Apply topical analgesic
  • Parents present
148
Q

See L16 cases

A

See L16 cases

149
Q

Laboratory markers of inflammation/inflammatory response

A
  • Increased WBC, CRP, ESR, procalcitonin
150
Q

Fever

A
  • 100.4 or 38 C
151
Q

Gold standard for temp

A
  • Rectal
152
Q

SIRS criteria for peds

A
  • 2 or more of the following:
    1. Temp > 38 or 90 OR 2SD above mean for age
    3. RR > 30 or 2SD above mean for age OR PaCO2 15K, 10% of WBC
153
Q

Newborn normal vital signs

A
  • HR: 120-160

- RR: 40-60

154
Q

What is sepsis? Severe sepsis? Septic shock? MODS?

A
  • Sepsis: SIRS + infection

- Severe sepsis: sepsis associated with organ dysfunction, hypoperfusion or hypotension (BP

155
Q

Define bacteremia?

A
  • Presence of viable bacteria in blood
156
Q

See cases from L17

A

See cases from L17

157
Q

Define early onset sepsis syndrome?

A
  • Sepsis in the first 6 days of time.
158
Q

Organisms typically responsible for early onset sepsis in newborn?

A
  • GEL mnemonic

- Group B strep, E. coli, Listeria monocytogenes

159
Q

Presentation of newborn sepsis

A
  • Poor feeding, decreased response to stimuli/lethargy, decreased tone, temp instability, vomiting/diarrhea, respiratory distress, CV instability, color changes
160
Q

Factors that increase risk for newborn sepsis

A
  • ROM > 18 hrs
  • Maternal chorioamnionitis
  • Maternal temp > 100.4 during labor
  • Previous infant with GBS
  • Maternal age
161
Q

What is chorioamnionitis?

A
  • Inflammation of fetal membranes. Diagnosed in mother who has fever during labor with two of the following: fetal tachy, uterine tenderness, foul vaginal discharge, maternal leukocytosis
162
Q

Define late onset sepsis in newborn?

A
  • Sepsis that occurs in a neonate that is greater than 7 days of age to 90 days of age
163
Q

Organisms typically responsible for late onset sepsis in newborn?

A
  • Coag neg staph, staph aureus, E. coli, Klebsiella, Enterobacter, candida, GBS, Serratia, acinetobacteria and anaerobes.
164
Q

Tx of early onset sepis?

A
  • Amp + aminoglycoside / 2nd generation cephalosporin
165
Q

Tx of late onset sepsis?

A
  • 2nd or 3rd generation cephalosporin + / or vancomycin
166
Q

Early sepsis presents with what? Late onset presents with what?

A
  • Early: pneumonia

- Late: meningitis

167
Q

What is occult bacteremia?

A
  • Bacteremia identified in patients without clinical evidence of sepsis (does not look ill) who have neither underlying chronic medical conditions nor clear foci of infection on exam and who are discharged to home after outpatient eval.
168
Q

Most common cause of occult bacteremia in 3mos-3yr age group?

A
  • Occult bacteremia. Most common bacteria = strep pneumo.
169
Q

Tx options for occult bacteremia

A
  1. Obtain a blood culture and give IM ceftriaxone prior to discharge
  2. Obtain WBC count. If > 15K, obtain blood culture and give ceftriaxone. This is Mett’s preference with added UA.
    - Either way: instruct to return if condition worsens
    - If negative culture at 48 hrs, stop abx. If pos, assess patient, finish workup and do abx for 10 days.
170
Q

What is meningococcemia? Presentation?

A
  • Presence of N. meningitidis in the bloodstream
  • Presentation:
    a. May present as occult bacteremia to severe sepsis and shock
    b. Sx: fever, PETECHIA/PURPURA, hypotension, emesis, lethargy, irritability
171
Q

Which individuals are susceptible to meningococcemia?

A
  • C5-9 complement deficiency
172
Q

Prognostic indicators for meningococcemia?

A
  • 90% mortality if 3 of following present:
    1. Petechia present for less than 12 hours prior to admission
    2. Hypotension
    3. Absence of meningitis
    4. Peripheral WBC
173
Q

Tx of meningococcemia

A
  • PCN G = drug of choice. Other alternatives = cefotaxime or ceftriaxone.
174
Q

Neonatal infections differential

A
  • Mnemonic = TORCHES

- Toxoplasmosis, other, rubella, CMV, herpes/hepatitis, syphilis

175
Q

Typical non-specific sx presenting with neonatal infections

A
  • SGA/IUGR
  • Thrombocytopenia
  • Hepatosplenomegaly
  • Jaundice
  • Microcephaly
176
Q

Where are toxoplasma gondii infections acquired?

A
  • CAT FECES, undercooked meat, uncooked eggs, unpasteurized milk
177
Q

Is there prenatal screening for toxoplasmosis?

A
  • No
178
Q

At what gestational age does risk of transmission increase? At what GA does disease severity increase?

A
  • Transmission risk increases as GA increases (most likely in 2nd/3rd)
  • Severity of disease increases earlier in GA
179
Q

Classic findings in neonatal toxoplasmosis infection

A
  • Classic triad = hydrocephalus, chorioretinitis, intracranial calcifications (diffuse or speckled; Mnemonic = toXo, X reaches out to all areas, ie. diffuse)
  • Majority with congenital disease lack signs clinically. May later develop seizures, learning disabilities, visual impairment, deafness etc.
180
Q

How is toxoplasmosis diagnosed?

A
  • Serum IgM titers or persistent IgG titers

- Optho exam, neuro exam, head CT (calcifications), LP (toxo PCR)

181
Q

Tx of neonatal toxoplasmosis?

A
  • Tx if infected, but asymptomatic. Meds = pyrimethamine, sulfadiazine, leucovorin, corticosteroids.
182
Q

Source of rubella infections

A
  • Humans ONLY. Spread vertically or through respiratory droplets.
183
Q

Most common vaccine preventable cause of birth anomalies worldwide

A
  • Congenital rubella syndrome
184
Q

Is there prenatal screening available for rubella?

A
  • Yes and recommended
185
Q

Classic findings in congenital rubella syndrome

A
  • Most common isolated sequela is hearing loss

- Class triad = deafness, cataracts, congenital heart disease (typically PDA and pulmonary stenosis)

186
Q

How is congenital rubella syndrome diagnosed?

A
  • First year of life!
  • Culture (nasopharyngeal swab, blood, urine, CSF)
  • Serum IgM
  • Rise in IgG titers
  • RTPCR
187
Q

Treatment of congenital rubella syndrome

A
  • None (tx = vaccine). Referral to specialists (OT/PT, neuro, audiology, cardiology and opthalmonology)
188
Q

What is the most common congenital infection in developed countries?

A
  • CMV

- Leading cause of sensorineural hearing loss in developed countries

189
Q

Is prenatal screening for CMV recommended?

A
  • No
190
Q

Classic findings in neonatal CMV infection

A
  • Petechia / ecchymosis, jaundice at birth or within a few hours (remember, physiologic jaundice = days 2-5), hepatosplenomegaly
191
Q

Diagnosis of CMV

A
  • Urine CMV culture, serum IgM titers, head CT with periVentral (cmV mnemonic) calcifications
192
Q

Tx for neonatal CMV

A
  • Ganciclovir
193
Q

Classic findings in neonatal HSV infection

A
  1. Disseminated disease (50% of cases, most commonly after 3 days of age): skin symptoms, poor feeding, lethargy, fever, convulsions, DIC, apnea and shock. Involves most commonly liver and lungs. Worst prognosis.
  2. SEM (1st or 2nd week of life): skin, eye, mouth
  3. CNS dz (2nd week of life): irritability, lethargy, poor feeding, tremulousness, seizures
194
Q

How is neonatal HSV diagnosed?

A
  • Culture (vesicles, nasopharynx, rectum, urine, conjunctiva, CSF) OR PCR!
  • Tzanck smear
  • CBC, LFTs (transaminases elevated in disseminated dz)
195
Q

Tx for neonatal HSV

A
  • IV acyclovir. Even with tx, overall mortality is ~20%.
  • Note: 85% of HSV infected infants acquire this from maternal genital tract, but only up to 35% of mothers who gave birth to HSV infected babies gave a history of genital herpes. Implication: do a good history.
196
Q

How do most congenitally derived hepatitis B infections present?

A
  • Most chronic. Typically asymptomatic at birth.
197
Q

Stages of syphilis

A
  1. Primary: painless ulcer/chancre on genitals
  2. Secondary: rash (palms, soles), fever, malaise, LAD, condyloma lata
  3. Tertiary: gumma formation, bone/skin/visceral changes
    - Latent w/o sx. Neurosyphilis can occur at any stage.
198
Q

Classic findings in neonatal Syphilis infection

A
  • Weeks to months post birth: Mucocutaneous lesions, LAD, rash, osteochondritis, snuffles (d/t hemorrhagic rhinitis)
  • Late sx: Hutchison teeth, anterior bowing of tibias, deafness, MR, frontal bossing, saddle nose
199
Q

Is prenatal screening for syphilis recommended?

A
  • Yes
200
Q

Tx for neonatal syphilis

A
  • If mother rec’d tx: do thorough PE until quantitative VDRL/RPR neg
  • If mother rec’d inadequate tx: same as above + LP, long bone x-rays, optho exam, CBC. Tx with penicillin!
201
Q

Risk of infection/transmission for infant born to seropositive HIV mother without tx? Tx with perinatal AZT?

A
  • Without tx: 25-30% (half in utero or during birth, other half from breast feeding)
  • With tx: 8%
202
Q

Classic findings in neonatal HIV infection

A
  • Sx develop bw 12-18 months
  • LAD, hepato/splenomegaly, FTT, oral candidiasis, recurrent diarrhea, recurrent opportunistic infections, hepatitis, cardiomyopathy, CNS disease
203
Q

How is neonatal HIV infection diagnosed?

A
  • PCR preferred. 93% will be pos by 2 weeks. 2 positive tests needed, not including 2 day test.
204
Q

Tx for neonatal HIV infection

A
  • ARV. Tx should be conducted by specialists.

- Avoid breastfeeding esp in developed countries!

205
Q

Which STIs are on the rise per CDC 2013?

A
  • Syphilis (including congenital)
206
Q

Avg age of coitarche in US? Avg # of partners in US high school grad? Avg age of sexual abuse?

A
  • Coitarche in US: 17 years
  • # partners: 4
  • Avg age of sexual abuse: 9
207
Q

When is screening for GC (gonorrhea) and CT (chlamydia) recommended?

A
  • Annually if sexually active and 25 with RF
208
Q

When is screening for hep C recommended?

A
  • One time testing if born bw 45-65 and unk status. RF = HIV, IV drugs, clotting factor recipient
209
Q

When is HIV screening recommended?

A
  • At least once age 13-64 yo. Annual if RF (IV drug, sex for drugs/money, HIV infected partner, MSM, preconception). Opt-out screening ideal.
210
Q

When is syphilis testing recommended?

A
  • Risk factors: exchange sex for drugs or money, IV drug use, entering detention facility, live in high-prevalence area
211
Q

5 Ps of STD prevention

A
  • Partners, prevent pregnancy, protection from STDs, practices, past hx of STDs
212
Q

STIs reportable in ALL states? IA?

A
  • ALL states: GC, CT, syphilis, HIV, AIDS

- IA: above + hepatitis A -> E

213
Q

When is Hep B vaccine recommended?

A
  • All unvaccinated, uninfected persons being evaluated for STD (safe in pregnancy!)
  • Give those with post-exposure HBIG + vaccine
  • CDC strategy: routine screening of all pregnant women, immunoprophylaxis for infants born to HBsAg+ve or unknown status mother, routine infant vaccine, vaccinate children
214
Q

Who should get HepA vaccine?

A
  • MSM, chronic liver dz, illicit drug users
215
Q

Who should get HPV vaccine?

A
  • CDC recommends giving Gardasil to 11-12 year old females and males. Can be administered up to age 26.
216
Q

Against what serotypes of HPV does Gardasil protect against? What does each serotype cause?

A
  • 6, 11, 16 and 18
  • 6 & 11 causes 90% of condyloma
  • 16 & 18 causes 70% of cervical cancer
217
Q

Which male condoms are best at preventing risk of transmission for STDs?

A
  • Latex
218
Q

Why are condoms with spermicide not recommended?

A
  • Increase in UTIs
219
Q

Which type of lubricants are better with condoms?

A
  • Water-based, not oil based
220
Q

When should most testing for STDs be done in pregnancy if at high risk? What is high risk?

A
  • 3rd trimester

- High risk: illicit drug use, STD during pregnancy, multiple partners during pregnancy, infected partner

221
Q

Most common cause for genital ulcer in US?

A
  • Herpes, also most common STI in women
222
Q

What should you test for if patient is positive for H. ducreyi chancroid?

A
  • This is a risk factor for HIV transmission. Test for HIV.
223
Q

SSx of chancroid

A
  • Painful genital ulcer, inguinal LAN, no e/o syphilis or HSV.
  • Not rule out diagnosis. Must rule out syphilis and HSV.
224
Q

Which herpes simplex virus has less recurrences?

A
  • HSV-1
225
Q

Which herpes infection has the highest risk for transmission to fetus?

A
  • Primary. No abs to HSV1 & 2 when HSV is diagnosed. Has 50% transmission.
  • Reactivation has 0-4% transmission risk
226
Q

When is c/section indicated in HSV infected pregnant mother?

A
  • If prodromal symptoms (tingling/burning in area where outbreaks have occurred) or active HSV lesions.
  • Mothers also must stop having sex with HSV infected partners.
227
Q

What is Jarisch-Herxheimer reaction?

A
  • Acute febrile rxn with HA, myalgia w/in 24 hrs of tx for syphilis. In pregnancy, may induce labor or cause fetal distress.
228
Q

Tx for syphilis is typically done with PCN. What is the tx in PCN allergic pt if pregnant?

A
  • Still requires PCN; however, needs to be desensitized via inpatient.
229
Q

US findings with congenital syphilis

A
  • Hepatomegaly, ascites, hydrops, thickened placenta (aka mega placenta)
230
Q

Sx of vaginitis

A
  • Discharge, malodor, pruritus, burning, swelling, dyspareunia, dysuria
231
Q

DDx for cervicitis

A
  • Chlamydia, gonorrhea, trichomonas, BV, douching, exposure to chemical irritants
232
Q

Most frequent reported ID in US

A
  • Chlamydia
233
Q

Sx of chlamydia infection

A
  • 75% are asymptomatic!

- Abnormal discharge, cervicitis, DUB (dysfunctional uterine bleeding)

234
Q

SSx of neonatal chlamydia infection

A
  • Conjunctivitis 5-12 days after birth

- Pneumonia

235
Q

Tx of gonorrhea.

A
  • Tx with ceftriaxone plus azithromax regardless of chlamydia status
236
Q

Ssx of disseminated gonococcal infection

A
  • Petechial / pustular acral (extremity) lesions, asymmetrical arthralgia, tenosynovitis, septic arthritis
  • SSx related to endocarditis and meningitis
237
Q

How do gonococcal infections present in infants? Tx?

A
  • Opthalmia neonatorum: perforation of globe and blindness manifesting 2-5 days after birth
  • Tx with erythromycin opthalmic ointment.
238
Q

How is PID diagnosed?

A
  • Easy to make diagnosis
  • Pelvic/lower abdominal pain, no other cause of pain, CMT (Chandelier sign) or adnexal tenderness. Additional supporting criteria = fever, mucopurulent d/c, increase WBC in vaginal secretions, increase ESR/CRP and GC/CT positive. Don’t have to have STD to have PID diagnosis.
  • Specific criteria = endometrial biopsy, TVUS or MRI, lap findings
239
Q

Tx guidelines for PID

A
  • Cover GC/CT, anaerobes (Bacteriodes), BV
240
Q

When is it necessary for PID tx to be inpatient?

A
  • Surgical emergency not excluded, pregnancy, non-compliant, unable to tolerate PO meds, tuboovarian abscess
241
Q

What is granuloma inguinale (donovanosis)? SSx? Diagnosed?

A
  • Genital ulcerative dz caused by Klebsiella granulomatis (gram neg) typically found in tropical and subtropical areas.
  • SSx: painless, progressive ulcerative lesions without regional LAD
  • Dx: dark-staining Donovan bodies
242
Q

What is lymphogranuloma venereum? SSx? Diagnosed?

A
  • Ulcerative dz caused by Chlaymdia trachomatis seen in Africa, India, SE Asia, S. America and Caribbean
  • SSx: painless ulcer, unilateral inguinal/femoral LAD, abscess, fistula, stricture, elephantitis
  • Dx: culture/direct immunofluorescence or NA test
243
Q

When is a c-section indicated for HPV in pregnancy?

A
  • Obstructed pelvic outlet, concern for excessive bleeding
244
Q

SSx of trichomonas infection

A
  • Diffuse, malodorous, yellow-green discharge with vulvar irritation, strawberry cervix
245
Q

Tx for trichomonas

A
  • Metronidazole (Flagyl)
246
Q

SSx of molluscum contagiosum. Tx?

A
  • Painless lesions with indented/umbilicated center. Tx = scoop out center.
247
Q

Common etiologies of cystitis

A
  • E.coli (up to 95%). Others = proteus, Klebsiella, staph saprophyticus
248
Q

Risk factors for cystitis

A
  • Common in sexually active women, recent intercourse, spermicide use, h/o UTI, menopause
249
Q

SSx for cystitis

A
  • Dysuria, frequency, urgency, suprapubic pain, hematuria
250
Q

SSx for pyelonephritis

A
  • Fever, chills, flank pain, CVAT, n/v
251
Q

How is cystitis/pyelonephritis diagnosed in terms of labs?

A
  • UA: leuk > 10 / hpf, nitrite >= 10^5 CFU/ml

- Culture pos

252
Q

Do Q&A for L19

A

Do Q&A for L19

Infectious Disease & Public Health (2 decks)

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