W3P2 Flashcards

Question 1

Q

What makes a successful STI?

Answer

A

Attachment to the mucosal cell surface
eg. using pili (gonorrhea)

Local invasion and proliferation while evading the host immune system
eg. by replicating intracellularly in epithelial cells and neutrophils (gonorrhea)

+/- Systemic dissemination

Some hosts are infected without symptoms

Question 2

Q

What is the Organism and Description for

a. Gonorrhea “the clap”
b. Chlamydia

Answer

A

a. Gonorrhea “the clap”
Neisseria gonorrhoeae -Gram-negative diplococcus
Bacteria

b. Chlamydia
Chlamydia trachomatis - Intracellular; lack normal cell wall (no peptidoglycan)
Bacteria

Question 3

Q

What is the Organism and Description for

a. Syphilis
b. Herpes

Answer

A

a. Syphilis
Treponema pallidum - Small, spiral-shaped organism
Bacteria/Spirochete

b. Herpes
Herpes Simplex Virus (HSV 1 + 2)- DNA virus, Herpes viridae family
Virus

Question 4

Q

What is the Organism and Description for

a. HPV, genital warts
b. Tichomonas “Trich”

Answer

A

a. HPV, genital warts
Human Papilloma Virus (HPV; many different types)- DNA virus

b. Tichomonas “Trich”
Trichomonas vaginalis- Flagellated, motile eukaryote

Question 5

Q

Which organisms cause Urethritis/ cervicitis

Answer

A

Neisseria gonorrhoeae
Chlamydia trachomatis
Trichomonas vaginalis

Question 6

Q

Which organisms cause Genital Ulcer Disease

Answer

A

Herpes Simplex Virus
Treponema pallidum
(Chlamydia trachomatis, certain serovars-> LGV)

Question 7

Q

Which organism causes genital warts?

Answer

A

Human Papilloma Virus

Question 8

Q

Presentation of Urethritis, Cervicitis, Procitits?

Answer

A

“ It hurts when I pee” = Urethritis

“ I have vaginal discharge” = Cervicitis

anal irritation, hurts when poo = proctitis

Question 9

Q

Differential diagnosis for Urethritis, Cervicitis, Procitis?

Answer

A

Neisseria gonorrhoeae
Chlamydia trachomatis
Trichomonas vaginalis

Question 10

Q

Transmission of Neisseria Gonorrhoeae

Answer

A

Gram-negative diplococci

Transmission via sexual contact
genital /anal
oral

Question 11

Q

Gonorrhea is easily treated, so what’s the big deal?*

Answer

A

Complications of N. gonorrhoeae:

Epididymitis: swelling of scrotum
Pelvic Inflammatory Disease: Chronic inflammation → adhesions within genital tract → infertility
Perihepatitis = Fitz-Hugh Curtis Syndrome (abdominal pain)

all these result from leaving it untreated. sometimes people are asymptomatic and don’t know something is wrong

Question 12

Q

Which is the most common STI

Answer

A

Chlamydia

Question 13

Q

What is a emphasized site of infection for N.gonorrhoeae

Answer

A

ARTHRITIS
Is a common extragenital complication of gonorrhea
I.e. wrist pain
it can still, but rarely can affect heart, brain, Gut etc.

Question 14

Q

Disseminated Gonnococcal infection

Triad of:

Answer

A

1) polyarthralgia/arthritis
2) dermatitis
3) tenosynovitis

Question 15

Q

How to diagnose Gonorrhea

Answer

A

NAATs (nucleic acid amplification test)
approved for urine/urethral/vaginal/cervical specimens (but used also for rectal, pharyngeal specimens)
- commonly used^

culture: hard
Gram stain: from purulent urethritis in men

Question 16

Q

Treatment for Gonorrhea

Answer

A

First there was penicillin→ resistance
….then there were fluoroquinolones
→ resistance (~28% in Canada, 2014)

Now, for acute urethritis:
Combination therapy recommended
Ceftriaxone (intra-muscular) x 1 dose, or
Cefixime (by mouth) x 1 dose

	Plus Azithromycin x 1 dose

Question 17

Q

Chlamydia trachomatis

gram stain, description
mechanism
symptoms

Answer

A

Small Gr – rods with no peptidoglycan layer in cell wall
Intracellular; infects epithelial cells
Different life cycle than other bacteriae
Chlamydia trachomatis serovars D-K
Majority of people infected: asymptomatic

Question 18

Q

Clinical Manifestations of Chlamydia

Females vs Males

Answer

A

Females:
Asymptomatic
Cervicitis
Vaginal discharge
Dysuria
Lower abdominal pain
Dyspareunia
Proctitis
Pelvic inflammatory disease
Perihepatitis

Males:
Asymptomatic
Urethral discharge
Urethral itch
Dysuria
Testicular pain
Proctitits

Question 19

Q

Diagnosis of C. trachomatis

Answer

A

Chlamydia
- very hard to culture (not done routinely)
- Thus : NAATs (nucleic acid amplification tests) is the go to
high Sn and Sp (higher Sn than culture)
use for urine, urethral or cervical specimens (and sometimes vaginal, rectal, pharyngeal specimens)

Question 20

Q

Treatment for Chlamydia

Answer

A

Adults with genital disease:

Azithromycin (oral) x 1 dose, OR
Doxycycline (oral) for 7 days

Question 21

Q

Trichomonas vaginalis 

- organism

Answer

A

The last one that drips^

- Urogenital protozoa
parasite
- flagella

Question 22

Q

Trichomonas vaginalis

- Clinical presentations

Answer

A

Vaginal discharge
Erythema of vulva and cervix
Itch
Dysuria
10-50% asymptomatic; most who have symptoms are women (many men asymptomatic)

Question 23

Q

Typical “strawberry” appearance of cervix

is associated with which infection?

Answer

A

Trichomonas Vaginalis

Question 24

Q

Diagnosis of Trichomonas Vaginalis

Answer

A

Microscopy of vaginal/urethral discharge for characteristic trophozoites

Antigen detection kits

NAAT

Question 25

Q

Treatment for Trichomonas Vaginalis

Answer

A

Metronidazole

aka flagyl, used for parasites

Question 26

Q

Genital Ulcer Disease

patient descriptions
DDX

Answer

A

“ I can see something down there…”
“ I have a rash”

DDx:			
HSV 1, 2
Treponema pallidum
Lymphogranuloma venereum 					
(= serovars L1, L2, L3 of Chlamydia trachomatis)

Question 27

Q

Herpes Simplex Virus 1&2

organism type
most transmission happens when?
timeline of infection
how long does the infection last

Answer

A

Herpesviridae family (DNA viruses)

Very common (seroprevalence studies: 15-50% positive)

Classically: HSV-1 = orolabial disease, HSV-2= genital: not true any more

Most transmission is during asymptomatic shedding

Establishes latent infection in the sacral sensory ganglia → periodic reactivation

Infection is for life

Question 28

Q

Clinical Manifestation of Herpes

Answer

A

Cluster of vesicles on an erythematous base: painful
Lesions anywhere in ‘boxer short’ area

Primary genital herpes
Sometimes extensive vesiculo-ulcerative lesions:
	lesions are PAINFUL!
Systemic symptoms (fever, muscle aches)
Tender lymphadenopathy
Meningitis (rare)

Question 29

Q

Diagnosis of HSV

Answer

A

Culture [not anymore]

PCR

Direct fluorescent Antibody (DFA) staining

Question 30

Q

Treatment of HSV

Answer

A

It is NOT curable

Medical treatment for clinically important first episodes and recurrences with either Acyclovir, Famciclovir or Valacyclovir

Can consider daily suppressive therapy for people with frequent recurrences (this also decreases transmission to partners)

Question 31

Q

Syphilis epidemiology

- mode of transmission

Answer

A

Least common of the 3 provincially reportable bacterial STIs
Incidence rising

Transmission via vaginal, anal, and oral sexual contact

Question 32

Q

Syphilis can be more complicated to recognize and diagnose than other STIs. Why?

Answer

A

different stages of disease (primary, secondary, latent, tertiary, etc). Can live in body and cause problems for decades!
different clinical manifestations at each stage of disease (“the great masquerader”), because it can spread to many organs in body
diagnosis can be complicated (no culture, PCR not widely used)

Question 33

Q

Stages of Disease of Syphilis

Answer

A

Transmission: sexual, congenital
+
Primary Syphilis
Secondary Syphilis: disseminated in skin, lymph nodes, etc commonly and classically found on the palms and soles

Latents syphilis is ASYMPTOMATIC
Early latent [within 1 year]: no symptoms
Late latent [over 1 year] low transmissibility, no symptoms
Tertiary Syphilis [years later] = aortitis, neurosyphilis

Question 34

Q

Chancres are found in what stage of syphilus

Answer

A

Primary Syphilis

this is a PAINLESS ulcer

Question 35

Q

What stage of syphilius would you see Gumma

Answer

A

Teriary Syphilis

Serpiginous Gummata of forearm
like full mouth bite mark shape

Question 36

Q

Syphilis Diagnostics

Answer

A

Mostly based on serology

Dark field microscopy of chancres

Question 37

Q

2 algorithms for Syphilis Serology

Answer

A

Screen with non-treponemal test (VDRL, RPR) and confirm with treponemal test
Screen with treponemal test (EIA), then perform non-treponemal test, then confirm with another treponemal test

Question 38

Q

Non-Treponemal Tests

Answer

A

measure antibodies in patients serum to cardiolipin antigen

Venereal Disease Research Lab test (VDRL)
Rapid Plasma Reagin (RPR)

Aggregation of Cardiolipin antigen in presence of antibody = positive test result for syphilis

this type of test is NON specific, so you get a lot of false positives*

Question 39

Q

Treponemal Tests

Answer

A

Syphilis Serology

measure antibodies against specific T. pallidum antigens
These tests are very SPECIFIC for T. pallidum
Enzyme-linked Immuno-Assay (EIA)
agglutination tests eg. Treponema Pallidum Particle Agglutination assay (TPPA)
Line immunoassay (LIA)

Question 40

Q

Syphilis Serology Interpretation
RPR or VDRL: Positive
TPPA: Positive

Answer

A

Interpretation:
Syphilis (any stage)
Previously treated disease (soon after trtmnt)

Question 41

Q

Syphilis Serology Interpretation
RPR or VDRL: Positive
TPPA: Negative

Answer

A

False Positive

Question 42

Q

Syphilis Serology Interpretation
RPR or VDRL: Negative
TPPA: Negative

Answer

A

No syphilis

Very early disease (need to repeat VDRL in 2-4 weeks)

Question 43

Q

Syphilis Serology Interpretation
RPR or VDRL: Negative
TPPA: Positive

Answer

A

Some cases of late stage disease

Previously treated disease (late after trtmnt)

Question 44

Q

Syphilis Serology First Algorithm

Answer

A

Start with non-treponemal test (RPR, VDRL) then confirm positives with treponemal test

Question 45

Q

Syphilis Serology 2nd algorithim

Answer

A

Start with treponemal test (EIA), then if positive perform non-treponemal test.
(If discordant, confirm with a second treponemal test)

Question 46

Q

Treatment of Syphilis if:
Primary, Secondary, or early latent
Late Latent, tertiary
Neurosyphilis

Answer

A

Penicillin is the treatment, dosage changes/increases

Primary, Secondary, or early latent: Penicillin IM x 1

Late Latent, tertiary: Penicillin IM weekly x 3 doses

Neurosyphilis: Penicillin IV for 10-14 days

Question 47

Q

LGV: Lymphogranuloma Venereum

- Clinical Presentation

Answer

A

Chlamydia trachomatis serovars L1, L2 and L3
Relatively rare
Outbreaks starting in 2003 (risk factor: MSM)

Clinical Presentation;
genital warts
often single painless papule
weeks later: tender adenopathy

Question 48

Q

HPV: Human Papilloma Virus

prevalence
which types cause warts
which cause precancerous lesions
prevention?

Answer

A

Very common (~70% adults have at least 1 HPV genital infx)

[More than 130 HPV types]
Types 6 and 11 commonly cause condyloma acuminata (genital warts)
Types 16 and 18 commonly cause (pre)cancerous lesions: cervical CA, anal CA

Vaccine now given in all provinces in grades 4-7

Question 49

Q

Treatment for HPV

Answer

A

Cryotherapy
Topical agents
Cervix: Colposcopy +/- excision procedures for pre-malignant/malignant lesions

Question 50

Q

Endovascular Infection includes:

Answer

A

Direct infection of blood and its components
Bacteremia, viremia, fungemia
Ehrlichia/Anaplasma
Plasmodium, Babesia, Trypanosoma, Leishmania
Infection of endovascular device
Prosthetic cardiac valve, PPM, ICD, CVL, AV fistula/mesh, vascular graft, LVADs, mechanical heart
Direct infection of vasculature and structures
Suppurative thrombophlebitis
Endarteritis
Endocarditis

Question 51

Q

Acute Infective Endocarditis

Answer

A

Abrupt toxic course lasting days to weeks

Question 52

Q

Subacute infective Endocarditis

Answer

A

Indolent protracted course featuring systemic symptoms often lasting longer than weeks

Question 53

Q

Shifting Age Distribution for Infective Endocarditis

Answer

A

Change in the nature of underlying heart diseases: rheumatic → DEGENERATIVE

Population is aging, aged with heart disease survive longer

Aged with heart disease benefitting from PROSTHETIC VALVE replacement surgeries

“health-care associated” IE due to increased uses of endovascular technologies
- IV catheters, hyperalimentation lines, dialysis lines/shunts,
- PPMs/ICDs
Biofilm formation

Question 54

Q

Predisposing factors to Infective Endocarditis

Answer

A

Native Valve (i.e the valves with which you are born)
Rheumatic heart disease
Congenital heart disease (some but not all)
Degenerative heart disease
Mitral valve prolapse
- Uncontrolled bacteremia and/or history of prior endocarditis
Prosthetic Valve (i.e the synthetic valve placed during cardiac surgery)
Endovascular device utilization
Intravenous access: long standing CVAD&raquo_space;» peripheral IV
Implanted devices, surgical materials
IVDU
intravenous drug use

Question 55

Q

Pathogenesis of Infective Endocarditis

Answer

A

Adherence -> Colonization [bcterial division, fibrin deposition, platelet aggregation, extracellular proteases, protection from neutrophils]
-> Mature vegetation

Many things can lead to adherence:
trauma, turbulence, metabolic changes
Bacteriocins, IgA protease, bacterial adhereance

Question 56

Q

Which area of the heart is MOST affected by Infective Endocarditis

Answer

A

Mitral Valve: 30-45%
Aortic: 5-35%

other two quite rare

Question 57

Q

Transient Bacteremia

Answer

A

When heavily colonized mucosal surfaces are traumatized
Degree of bacteremia is proportional to the burden of colonization and degree of trauma

Typically “low grade” and “transient”

≤ 10 CFUs/ml
Blood stream sterilized within 30 minutes
- Function of “serum susceptibility” of the organism

Sufficient to infect a NBTE valvular lesion

Question 58

Q

Virulence Factor Dextran:

Answer

A

Complex extracellular polysaccharide, “glycocalyx”
Role in dental caries (S. mutans)
Prominent among certain Streptococcus spp.
Promotes adherence to platelet-fibrin matrix (NBTE)

Question 59

Q

Virulence FActor: Adhesion to markers of Damaged Endothelium

Answer

A

Fibronectin

S. aureus binding and uptake into “normal” endothelium, followed by triggered apoptosis
Clumping factor, coagulase

Question 60

Q

Virulence Factor: Bacteria-platelet-aggregates in circulating blood

Answer

A

Staphylococcus spp. (surface receptor-fibrinogen-platelet receptor, or via vWF system)
Streptococcus spp. (surface Antigens-IgG-platelet FcR)
↓ rate of removal of organism
↑ adherence and aggregation on vegetations

Question 61

Q

Virulence Factor Disruption

Answer

A

Utility of prophylactic antibiotics

Even sub-inhibitory (prophylactic) antibiotics may prevent IE by
a. Decreasing expression of adhesion virulent factors
b. Direct cell killing

Question 62

Q

Describe within the Vegetation of Infective Endocarditis

Answer

A

Minimal phagocyte infiltration
Protected from circulating immune factors
Environment for major proliferation

Deeper dormant/inert bacterial forms  (may represent up to 90% of bacterial burden)

Question 63

Q

Microbiology of IE for a Native Valve

Answer

A

Native Valve

Community acquired

Staphylococcus aureus / viridans Streptococcus spp.
Lesser extent Enterococcus spp.

Nosocomial

Staphylococcus aureus
Lesser extent Enterococcus spp.

IVDU

Staphylococcus aureus
Lesser extent other bacteria

Question 64

Q

Microbiology of IE for a prosthetic Valve

Answer

A

Early post surgical, intermediate Post surgical (2-12 months)

coagulase NEGATIVE STAPH > staph aureus

Answer 65

A

Considered in microbiology of culture negative endocartitis

HACEK

Gram negative organisms with unusual growth charcteristics
Not truly “culture negative” using modern techniques

HACEK is an acronym for a group of organisms that are small, fastidious gram-negative bacilli. 1. The HACEK organisms include Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae.

Answer 66

A

FEVER 80%
Chills
Weakness
Dyspnea

SIGNS:
fever 90%
heart murmur 85%
* important to do cardiac Auscultation

Answer 67

A

Most important diagnostic test is BLOOD CULTURE

When bacteremia present, first two cultures yield agent > 90% of the time
Can be altered if ABX are given prior to culturing
Recommended
3 sets, only 2 bottles per stick in first 24 hours
At least 10 ml of blood in each bottle
May need prolonged incubation

Answer 68

A

TTE- transthroacic echo?

Utility in all patients suspected of having endocarditis (usually by agent and syndrome)
May be technically inadequate in up to 20% of individuals
Variable sensitivity
Negative study cannot R/O IE
Highest in right sided IE due to positioning of the heart
False positive studies are rare

TEE- trans esophageal echo?
Invasive
More sensitive than TTE (65% vs 95%)
Should be considered in suspected cases where TTE was negative
Especially useful for prosthetic heart valves, intracrdiac abscesses and fistulae
Negative results do not exclude IE
May repeat TEE in 7-10 days

Answer 69

A

Used to diagnose Definite vs Possible IE

Definite IE:
Pathologic Criteria
Microorganisms: demonstrated by culture or histology in a vegetation, OR in a vegetation that has embolized, OR in an intracardiac abscess, OR
Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis
Clinical criteria
2 major OR 1 major and 3 minor OR 5 minor

Possible IE:
- 1 major and 1 minor or 3 minor

Rejected:
Firm alternative diagnosis, OR
Resolution of manifestation of IE with ABX for 4 days or less, OR
No pathologic evidence of IE at surgery or autopsy, after ABX therapy for 4 days or less
Does not meet criteria for possible IE

Answer 70

A

Blood culture positive for IE (at least one of:)
a. Typical microorganisms consistent with IE from 2 separate blood cultures:
- Viridans streptococci, S. bovis, HACEK group, S. aureus
- Community acquired enterococci, without primary focus
b. Microorganisms consistent with IE from persistently positive blood cultures

Evidence of Endocardial Involvement

a. Echocardiogram positive for IE (TEE recommended in patient with prosthetic valves, rated at “possible IE” by clinical criteria, or complicated IE/paravalvular abscess)
b. New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient)

Answer 71

A

a. Predisposition: predisposing heart condition or injection drug use
b. Fever: T>38C
c. Vascular phenomenon: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
d. Immunologic phenomenon: GN, Osler nodes, Roth spots, and positive RF

e. Microbiological evidence: positive blood culture but does not meet a major criterion as noted above, or serological evidence of active infection with organism consistent with IE
Echocradiographic minor criteria eliminated

Answer 72

A

Destruction of underlying heart valve
- Healing by fibrosis and calcification
Acute IE
Vegetation is larger, softer, more friable
Associated with more suppuration, more necrosis
Less healing
Valve perforation
Rupture of chordae tendonae, interventricular septum, papillary muscle
Perivalvular abscess
Fistula into pericardium, myocardium
Myocarditis, myocardial infarction, and pericarditis
Involvement of conduction system

Answer 73

A

1. Embolic phenomenon
15-35% of cases have clinical events
70-95% of cases had clinical events in pre-antibiotic era
Kidney, spleen, coronaries, brain
Immune phenomenon

Immune complex deposition
Complement activation
Autoimmune process activated by increased circulating antibodies

Answer 74

A

During active IE, all biopsies are found to have abnormal architecture

Abscess
Infarction
GN

Answer 75

A

Mycotic aneurysm

Can be prominent clinical presentation, or discovered at autopsy years later
More common with viridans Streptococcus

Mechanism

Direct invasion of arterial wall, abscess and/or rupture
(Septic) emboli occluding vasa vasorum
IC deposition and injury to the vascular wall

Tend to occur at bifurcation points

Answer 76

A

Cerebral emboli
Most common neurologic event in IE – 20%
MCA and branches most commonly involved
Hemorrhagic transformation of ischemic event is leading CNS related cause of death in IE

Other (non-exhaustive list)
Purulent meningitis – S. pneumoniae
Microabscesses – S. aureus

Answer 77

A

Enlargement
Immune stimulation, follicle engorgement

Infarction
44% of autopsies, usually clinically silent

Abscess
Surgical indication, or percutaneous drainage

Spontaneous Rupture

Answer 78

A

Typically associated with right sided IE (right heart supplies to lungs)

PE (septic or “bland”) ± infarction
Acute pneumonia
Pleural effusion
Empyema

Answer 79

A

Petechiae – 20-40%
Osler nodes (Immunologically mediated)
IC deposition in blood vessel
- arteriollar intimal proliferation with extension to venules and capillaries, may be accompanied by thrombosis or necrosis
- Tender, at pulp of fingers
Janeway lesions (Vascular event)
Septic emboli
- feature subcutaneuous abscesses
- Non-tender, palms and soles

Answer 80

A

Roth Spots
- Lymphocytes, edema and hemorrhage in nerve fibre layer of the retina
Conjunctival petechiae/hemorrhage
Flame hemorrhages

Answer 81

A

All components of immune system are deficient c/w immune system of older children/adults
Degree of deficiency is inversely related to gestational age and birth weight, but even term are deficient

Protection
Placenta, filters microorganisms
Maternal Ab, but mostly transferred in 3rd trim
Breast milk, contains secretory IgA

Answer 82

A

Most important is the time during gestation that the transmission of infection occurs
- During 1st trimester, while the fetus is being formed, the most devasting effects occur

Three types of effects:

Interference with normal development
Inflammatory reaction to the infection
Placental insufficiency leading to poor growth

Answer 83

A

THE MOTHER
Recognizing exposure of a pregnant woman
- Most of the time the pregnant woman are not symptomatic
- Detection of specific IgM Ab to an offending agent or rising titre of IgG are helpful in assessing risk
- Baseline immunity will help to exclude dx
I.e. was the mother already immune to Rubella, CMV, parvo, etc…

Answer 84

A

IgG crosses placenta, so not helpful
- Would be measuring mother’s Ab

Presence of specific IgM or rising IgG titre indicates fetal infection

Isolation of offending agents if possible

Viral cultures of urine and other body secretions for CMV, Rubella, HSV
PCR amplification if possible, ie. Toxo
Pathology of placenta
Darkfield microscopy from lesions for T. pallidum (syphillis)

Answer 85

A

Limited number of treatable infections.  Don’t want to miss these:
Toxoplasmosis
Syphillis
HSV
HIV
CMV

No effective treatment
Rubella

Answer 86

A

Toxoplasmosis
Avoid cat litter boxes, gardening, eating raw or undercooked meat

Rubella
Prenatal vaccination, or if non immune post delivery to protect future offspring

CMV
Meticulous handwashing

Syphillis
Serologic testing early on, and repeated if at risk for exposure. Of course treat pregnant mother to prevent infection in the fetus

Listeria (gram+)
Avoid Deli meats

Answer 87

A

CBC: yees has look for abnormalities (i.e. platelets are low)
Blood culture/Urine culture: bacterial infections would present acutely and this is not an acute presentation
CSF culture^
Torch screen: misconception, not effective THERE IS NO SUCH THING**
Immunoglobulins, specifically IgM (it doesn’t cross the placenta)

Answer 88

A

TORCH: Toxo, Other, Rubella, CMV, Herpes
^ just an acronym for screening general stuff

The common misconception
There is no ONE test that will screen for congenital infections
Congenital infections of different causes have many clinical similarities
The acronym “TORCH” should be expanded. “O”ther now includes
Syphillis, TB, Listeria, leptospirosis, Hepatitis B, enteroviruses, Varicella, Parvovirus, HIV…and most recently ZIKA!!
Nothing replaces a good clinical accumen and directed specific testing

Answer 89

A

Go by your index of suspicion!
Always start with your clinical history, and getting the OB/GYN report
- Ultrasounds, serologies AND when they were done. You will save a lot of time, effort and cost
A full work up should always include and ophthamology assessment

Answer 90

A

Classic Triad: Hydrocephaly, diffuse intracranial calcifications, chorioretinitis (inflammation in the eye)

Do maternal serology (IgG)
NEG: excludes Congenital Toxoplasmosis, mom was never infected.
POS: Titre and Avidity help us with timing
Only infection while pregnant will affect the baby

Do Toxo IgM, but stays positive for 6-18 months
NEG: Does not totally exclude, but unlikley
POS: Increases the likelihood, but + for >6 months

Answer 91

A

CHILD
Ophthamology: assess for chorioretinitis
Head imaging: CT vs Ultrasound vs Xray
PCR on whole blood, and CSF

MOM
Toxoplasmosis suspected during pregnancy
Seroconversion documented
Work up to assess if baby infected/affected
PCR on amniotic fluid
Serial ultrasounds, looking for ventricular dilatation
Placental histology
If work up indicates infection, then important to treat mom, which will also treat the fetus
Baby will need to continue treatment once born

Answer 92

A

Once the baby is born:
Check Mom’s rubella status PRIOR to the current pregnancy
POSITIVE: excludes Rubella
NEGATIVE/ or unknown
- Check Rubella IgG on Mom and/or baby
If negative: excludes Rubella, immunize Mom
If Positive: Do Rubella IgM on both Mom and baby
If IgM Positive: Congenital Rubella
If Negative: Do Rubella Viral Cultures
Isolation of the virus in the baby is proof positive

Answer 93

A

Once the baby is born:
Urine viral culture/PCR for CMV
POSITIVE: If done within first 2-3 weeks of birth, then can diagnose Congenital CMV
NEGATIVE: excludes CMV

While mother is still pregnant:
Serology IgG not helpful as most women have antibody (60-80%), indicating infection at some point during her life.
Complicated and controversial on how to diagnose in mother, but includes IgM and PCR

Answer 94

A

3 distinctive syndromes in the baby: Majority of infections start during delivery with incubation of 2 days to 6 weeks

Skin, eye, mucous membrane “SEM”
Encephalitis
Disseminated

If there are skin lesions: test the lesion (special stain, or PCR, or viral culture)
POSITIVE: Confirms Diagnosis

If there are no lesions:

Culture mouth, eye, urine, rectum
CSF and Blood for HSV PCR

Answer 95

A

SYPHILIS
Check maternal serology, and recheck at time of delivery, or thereafter
NEGATIVE: exclude
POSITIVE: Review history, prior treatment

This is not something you want to miss, as this plus congenital Toxo, HIV, HSV, CMV are really the only treatable causes!

Answer 96

A

Maternal primary CMV in pregnancy

43-58% transmit to fetus
15-20% of infected newborns are symptomatic
 - Mortality: 20-30%
 - Sequelae: 90% of survivors
       - Severe psychomotor delay 50-60%
       - Hearing loss 30-60%

80-85% are asymptomatic at birth
12-15% hearing loss, behavior or learning problems

Answer 97

A

17% of seropositive pregnant women shed virus at some point during the pregnancy
0.8-3.4% transmit to fetus
Symptoms and severe sequelae: extremely rare
Hearing loss: 5% (unilateral or mild)

Answer 98

A

Baby may have become infected at time of delivery or anytime afterwards. Only infection during pregnancy causes the hearing problems.

Therefore must find the virus when the baby is a newborn to say that this happened.

Answer 99

A

if exposed to this virus, must tell pregnant women:

About 30-60% of adults are immune
So if she was immune, there is no risk to the baby

In pregnancy: ?spontaneous abortion in 1st trimester; fetal anemia and hydrops in 2nd and 3rd trimester; ? Stillbirth
Causes bone marrow aplasia, resulting in severe anemia in the baby, and congestive heart failure
- Hydrops fetalis: abnormal accumulation of fluid in two or more fetal compartments, including ascites, pleural effusion, pericardial effusion, and skin edema.

Other infectious causes of nonimmune hydrops:
Toxoplasmosis, rubella, CMV, syphilis

Answer 100

A

Diagnosis: Serology on mom at time of exposure
If IgG positive: She is immune, and baby not at risk
If IgG negative, check and follow IgM, IgG
If there is seroconversion, then need to follow fetus, and can do fetal blood transfusions if necessary

Answer 101

A

Hepatitis B
If mother is sAg and eAg positive:
70-95% transmission, and 90% of infants will become chronic carriers
THEREFORE GIVE HBIG to the baby (HepB immuneglobulin), AND FIRST DOSE OF VACCINE AT BIRTH (then at 1, 6 months) protective in 85-95%
VACCINE ALONE protective in 70-80%

Hep C
Perinatal tranmission
Less than 5%
Increased if co-infected with HIV (18-20%)

Diagnosis in infant?
Follow serology at 6, 12, 18 months
?PCR

Answer 102

A

Highest risk of transmission if
First episode of maternal infection in pregnancy
- 40-50% transmission, versus 0-5% if recurrent
Multiple cervical lesions
Rupture of membranes > 6 hours
Instrumentation, scalp electrodes
Prematurity, no maternal antibody

Clinical presentation:

Skin-eye-mucous membrane (SEM)
Encephalitis
Disseminated

20 % HAVE NO SKIN LESIONS!!

Answer 103

A

Varicella Zoster Infection

VZV embryopathy:
- Limb scarring and atrophy
- Bony defects
- CNS abnormalities
- Eye, chorioretinitis
Development of Zoster early in life
Congenital varicella syndrome: 1-2%

Unlikely that VZIG (varicella immuneglobulin) is protective to fetus
Give VZIG to newborn if maternal varicella 5 days before, to 2 days after delivery
- Severe disease in newborn: mortality of 5 %

Answer 104

A

Up to 20% of women experience by age 30
>50% have at least 1 in a lifetime
10% of women have recurrent infections
Up to 20% chance of the cause of fever in feverish newborns
- High if uncircumcised male (20%)
- Approx 7% otherwise

Answer 105

A

Infections at any site:
Bladder, kidney or protate

Cystitis
Infection at level of bladder

Pyelonephritis
Infection involving renal parenchyma (kidney)

Renal abscess
Pus collection with severe pyelo or spread from blood stream

Bacterial Prostatitis
Infection of the Prostate gland

Answer 106

A

Higher incidence in females because of shorter distance from urethra to bladder

Most of the time bacteria is “flushed out” with the next void
Transport from bladder to kidney can result in pyelonephritis

Ascent to kidney facilitated by: 
Pili of the bacteria (E. coli)
Obstruction
Neurologic disease leading to a poorly functioning bladder
Pregnancy
Reflux (urine going up the ureters)

Answer 107

A

E.coli accounts for 85% (due to pathogenic factors)
- P Fimbriae/pili allow for bacteria to attach

Staph. Saprophyticus isolated in 5-15% of young women with UTIs

Other Enterobacteriaceae, enterococcus, yeast, Group B strep, account for the minority

Urea splitting organsims may form struvite stones
- Proteus, Morganella and Providencia
All bets are off in there is indwelling plastic, such as catheters
- Biofilm forms and traps unusual organisms

Answer 108

A

Most important is periodic, complete and normal voiding
Washes out bacteria, and cells to which they are attached

Behavioral risks
Sexual intercourse
Mechanically allows bacteria to ascend. Occurs 30% of encounters, but voiding clears the bacteria

Patients with structural or functional abnormalities of the Urinary tract that compromise voiding.

Obstruction to flow
Increased access (catheters)
Pregnancy (urinary stasis)

Answer 109

A

Uncomplicated Cystitis or Pyelonephritis
Lower tract symptoms
Dysuria (pain on voiding)
Frequency (frequent urination)
Urgency (“I need to go NOW!)
Discomfort in suprapubic or lower back area
Gross hematuria
Upper tract or Pyelonephritis
High fever
CVA (costo-vertebral angle) tenderness
Unlikely UTI if symptoms are in between voids and if there are vaginal symptoms

Answer 110

A

Young infants cannot complain of the typical symptoms
Fever, irritablility
Afebrile, but poor feeding; vomiting; diarrhea; jaundice; poor weight gain

Answer 111

A

Leukocyte esterase: detectsesterase, an enzyme released by white blood cells. Most sensitive
94% when UTI suspected
Specificity: 64-92% (due to other infection/inflammation of tract, urethera, vaginitis..)

Nitrite: Bacteria that cause a UTI make an enzyme that changes urinary nitrates to nitrites.
Sensitivity: 16-82%
Specificity: 95-100%, good to Rule-In

[Blood and/or protein
Poor sensitivity and specificity]

Answer 112

A

Microscopy: Technologist dependant
#WBC/HPF: Sensitivity: 32-100%; Specificity: 45-97%
Bacteria: Sensitivity: 15-96%; Specificity: 11-100%
If analyzed > 3 hours after collection: The sensitivity drops by 35%

Answer 113

A

Combination of tests maximize the Sensitivity and the Specificity

LE or nitrite +: Sens: 83-100%; Spec: 68-98%

Microscopy for WBC and bacteria:
- Sensitivity: 99%

Anything positive on dip/microscopy
- Sensitivity of 100%; Specificity poor

If dip/microscopy all negative
- Negative Predictive Value: 100%

Answer 114

A

Empiric therapy may need to be modified based on susceptibility testing

Antimicrobials excreted in urine are preferred

For cystitis, only urinary antibacterial activity is necessary

For Pyelonephritis, need adequate drug level in urine and tissue, and possible blood level

Answer 115

A

Usually treated empircally based on symptoms and dipstick result, and often cultures are not sent (adult medicine)
It takes 2-3 days to get urine culture results,and many treat for only 3 days
Send a culture if symptoms are uncertain, history of frequent relapse, or if pregnant
Most use TMP/SMX (Septra) for 3 days
Alternatives: Quinolone (Cipro) also for 3 days, or Nitrofurnatoin (local bacteriostatic) for 7 days

Answer 116

A

Can have bloodstream extension, so blood and urine cultures are indicated before treatment

Empiric therapy is based on severity, i.e oral vs. initial IV then oral or all IV.

Usually start with Ampicillin (to cover possible enterococcus) and aminoglycoside (To cover gram negatives: Genta/Tobra), and tailor based on urine C&S

For oral treatment, many use Septra or quinolone
Because both are extremely well absorbed (bioavailable)

If no improvement by day 3, consider a complicated infection (obstruction, abscess

Answer 117

A

Should not be treated except

Pregnancy: Can go onto pyelonephritis, which can precipitate premature labor
About to have a urological procedure: compromise of the mucosa can lead to the complication of spread to the bloodstream

Answer 118

A

2 episodes every 6 months, or 3 every year
Some refer to it as “Honeymoon cystitis”

Can try daily or alternate day low dose TMP/SXT, or following intercourse
- Reduces gram negative flora in periurethral area, but increase incidence of resistant UTIs

Nitrofurantoin has less of an impact on colonizing flora, but can intermittently sterilize the urine through high urinary antimicrobial levels

Answer 119

A

UTIs under 3 months

quite common!
higher if infant is febrile
uncircumsized males = higher

Answer 120

A

Incidence decreases in boys and increases in females during the first 6 months, and by age 1 females outnumber boys 3-10:1.

Answer 121

A

WORSE IN CHILDREN

May have no symptoms attributable to the urinary tract
Higher likelihood of having blood spread, and complications as meningitis (neonates)
Higher likelihood of having some malformation of the urinary tract
Therefore needs more extensive workup initially and in follow-up

Answer 122

A

Neonates have lower grade fever or afebrile
Fever is of shorter duration, and disappears more promptly on treatment
May just have poor feeding, lethargy, grunting, poor weight gain and no fever OR fulminant sepsis
Asymptomatic other than jaundice

Answer 123

A

Ascending vs Hematogenous
- not sure which comes first, chicken vs egg situation

A substantial proportion of newborns with UTI have bacteremia

Answer 124

A

Septra and Quinolone

Answer 125

A

If under 6-8 weeks of age: all have a septic workup including a lumbar puncture
Treated all IV if under 1 month
All newborns should have an ultrasound to rule out congenital malformations of the urinary tract
Consider radiographic work up with VCUG to detect reflux from bladder up the ureter, if the UTI is considered “atypical”
- Recurrent; Non E.coli; abnormal ultrasound; bacteremia
May require prophylaxis if there is high grade reflux, at least until the time they are toilet trained

Answer 126

A

Higher the grade, higher up the infection = worse

Answer 127

A

To detect dilatation, obstruction, anomalies
If a late prenatal ultrasound has been done, is this still a necessary test?
NEJM: Jan.16,2003 Hoberman et al
Ultrasound did not change management, nor did it differentiate those with or without reflux
There is no role for an U/S for every repeat UTI if the anatomy is known, and there is no unexpected response to treatment

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