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Clin Med > ID: Bacterial diseases > Flashcards

ID: Bacterial diseases Flashcards

1
Q

how long do you wash hands with soap and water

A

at least 20 seconds

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2
Q

vast majority of infections are causd by

A

microbes from normal flora

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3
Q

general stages of an infection (7)

A
  1. transmission
  2. evasion of host
  3. adherence to mucous mems
  4. colonization by growth of bacteria at the site of adherence
  5. disease s/s start and inflammation rxn
  6. host responses during steps 3-5
  7. progression or resolution of dz
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4
Q

MC site of entry for microbes

A

mucosal surfaces

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5
Q

mycobacterium is?

A

intracellular pathogen

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6
Q

what are direct and indirect measures for the acute phase response of an infection

they are very ____ but not ____ ?

which do you check weekly and which is daily?

A

ESR–erythrocyte sedementation rate—-weekly because its slow

CRP–C reactive protein—daily

assess PTs level of inflammation

very sensitive, not specific

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7
Q

staph

  • morpholoy
  • coagulase pos or neg
A

gram + cocci

coagulase + (contains the enzyme coagluase)

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8
Q

what does coagulase enzyme activate

A

thrombin— causes clotting

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9
Q

why are most staph aureus resistant to penicillin

A

because they contain the enzyme penicillinase—this inactivates PCN but not antibitoics like methicillin or naficillin—— aka Methicillin SENSITIVE staph aureus (MSSA)

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10
Q

how can MRSA be acquired

A

hospital or community

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11
Q

where can MRSA live in the body

A 
nasal passages
throat
skin 
***areas of colonization***
-these people can be carriers
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12
Q

PTs with MRSA have:

  1. higher ____
  2. longer _____
  3. higher ____
A

higher mortality
higher healthcare costs
longer hosp stays

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13
Q

HA-MRSA

  • RF (8)
  • when can you get it
  • complications
  • resistance to?
  • transmission
  • tx
A

RF:

  1. ABX use (esp fluoroquinolones, cephalosporins)
  2. prolonged hosp stay
  3. ICU stays
  4. hemodialysis
  5. proximity to others with MRSA
  6. chronic wound—-diabetes
  7. discharge with a central venous catheter or invasive device
  8. discharge to nursing home

> 48 hours after hospitalization or w/in 12MO of exposure to a HC setting

comps:
- bacteremia
- pneumonia
- skin/soft tissue damage–surgical site infections

Multi-drug resistant (more so than CA-MRSA)

transmission: via HC workers–contamination of hands and surfaces

TX:
1. IV vancomycin **
or
2. Linezolid

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14
Q

what is the leading cause of surgical site infection

A

HA-MRSA

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15
Q

CA-MRSA

  • define it
  • MC in?
  • sensitive to?
  • RF (10)
  • transmission
  • tx
A

MRSA infection w/o hx of HC setting exposure

MC in:

  1. young, healthy
  2. initially it was reported in IV drug users
  3. prisons, sports, childcare centers, military

sensitive to: beta-lactam ABXs

RF:

  1. skin trauma
  2. bbody shaving
  3. incarceration
  4. equipment sharing
  5. close contact with person with MRSA colonization or inf
  6. necrotizing pneumonia
  7. osteomylitis
  8. UTI
  9. endocarditis
  10. sepsis

transmission: surfaces that are contaminated

tx:
1. I/D for abscess
2.** PO clindamycin 300mg TID x7-10days
or
3. ***PO Trimethoprim-Sulfamethoxazole 1-2 tabs DS x 7-10days
or
4. Doxycycline 100mg BID x 7-10days

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16
Q

what is the most frequent cause of skin and soft tissue infections presenting to the ER

A

CA-MRSA

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17
Q

What causes the abscess formation seen with MRSA

A

protein seen with CA-MRSA

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18
Q

sepsis
vs
septic shock

A

SEPSIS:
uncontrolled inflammatory response
dysregulated host response to infection
life threatening organ dysfunction

SEPTIC SHOCK:

  • subset of sepsis
  • circulatory, cellular and metabolic dysfunction
  • assoc with higher risk of mortality
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19
Q 
septic shock 
-what s/s order--MC manifestation? 
-steps of progression
-what is an indirect marker? 
-diagnosis? 
-etiologies--MC? 
-RF (9)
-
A

hypotension–>tissue perfusion
lactate level= indirect marker for tissue perfusion
FEVER=MC MANIFESTATION

infection–>bacteremia–>sepsis–>septic shock–>multiple organ dysfunction–>death

clinical diagnosis

etiology: resp, GI, GU, and skin/soft tissue infections are MC sources
* **Pneumonia is MCC sepsis

RF:

  • bacteremia
  • > 65YO
  • immunosupp
  • DM
  • obesity
  • CA
  • CAP
  • previous hospitalizations
  • genetics
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20
Q

SIRS criteria
-stands for
-

A

systemic inflammatory response syndrome (SIRS)

no longer part of sepsis guidelines
but stil can identify acute infections

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21
Q

SIRS criteria

A

requires at least 2 of the 4:

  1. body temp less than 36 C or greater than 38 C
  2. Hr>90
  3. RR > 20/min
  4. WBC < 4,000 or greater than 12,000 OR greater than 10% bands
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22
Q

what repalced SIRS?

-used for? not used for?

A 
Quick SOFA (aSOFA)---outside ICU 
 SOFA--ICU

*used to predict mortality
NOT to diagnose sepsis

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23
Q

qSOFA criteria

A

must meet 2 of the following:

  1. new or worsened mentation
  2. RR > or equal to 22/min
  3. SBP < or equal to 100 mmHg
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24
Q

gram+ shock resutls from?

  • leads to?
  • etiologies
A

eXOtoxins–>fluid loss

  • staph
  • strep
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25
Q

gram - shock caused by??

-etiologies

A

enDOtoxins

  • e coli
  • klebsiella
  • proteus
  • pseudomonas
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26
Q

Neoantes

  • susceptible to what bacteria
  • how to tx
A

GBS**
E. coli
Klebsiella

TX:
Ampicillin + gentamycin
and/or
cefotaxime is added if gram- meningitis suspected

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27
Q

Children susceptible to what bacteria

tx?

A 
H. influenzae 
pneumococcus
meningococcus 
TX: 
3rd gen cephs 
vancomycin 
Clindamycin
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28
Q

adults are susceptible to what bacteria

A

gram+ cocci
aerobic bacilli
anaerobes

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29
Q

IVDU susceptivle to what bacetria

tx?

A

S. aureus

***VANCOMYCIN

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30
Q

Asplenic PT susceptible to what bacteria

A

pneumococcus
H. influ
meningococcus

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31
Q

Line associated infections?

A

skin flora

*coag negative staph

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32
Q

two sepsis biomarkers?

A

lactate levels

procalcitonin

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33
Q

when do procalcitonin levels rise in sepsis

-peaks?

A

w/in four hrs after onset of infection

PEAK at 12-48 hours

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34
Q

when do lactate levels rise in sepsis?

-what is a diagnostic level

A

secondary to tissue hypoxia

>18 is diagnostic for septic shock

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35
Q

what kind of acid-base disorders would you find with sepsis

A

respiratory alkalosis with a metabolic acidosis

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36
Q

how many sets of blood cultures do we need with a septic PT

A

two

*including a set from a central venous cath

37
Q

tx sepsis

A

ID and remove cause of infection
PT MC will need ICU admission

  1. fluid resuscitation is priority in early mng—IV crystalloid at 30mL per kg w/in first three hours
  2. empiric ABX within one hour—- Piperacillin-tazobactam + vancomycin for adults
  3. vasopressors: if hypotensive after fluid resuscitation—–norepinephrine is DOC
  4. send blood cultures (draw b4 ABX tx)
  5. remove all existing caths, IV lines and central lines
38
Q

what is the target MAP for septic pt

A

> 65 mmHg

39
Q

scarlet fever:

  • define
  • bacteria involved?
  • what kind of rxn
  • CM
  • population MC affected
  • % of PT who get it
  • diagnose
  • tx
A

diffuse skin eruption
etiology: Group A streptococcus (strep. pyogenes) infections

Type IV (delayed) hypersensitivity rxn to a pyrogenic strain—pyrogenic exotoxins

CM:
1. fever, chills, PHARYNGITIS*****

  1. rash: diffuse erythema that blanches with pressure + multiple small (1-2 mm) papular elevations with a SANDPAPER texture (very very small diffuse papular rash)
    - rash will spare the palms and soles
    - start at neck/upper trunk and groin–>spreads to extrems and trunk—-eventually will desquamate
  2. flushed face with circumoral pallor and strawberry tongue
  3. Pastia’s lines: linear petechial lesions seen with pressure points, axillary, antecubital, abdominal or inguineal areas

MC affects kids 5-15YO
peak incidence: winter and spring
develops in <10% of streptococcal throat infections (less common since development of PCN)

diagnose: rapid antigen test and throat cx

TX:

  1. PCN first line (po or im)
    * **Macrolide (azithromycin) or clindamycin if PCN allergic
  2. Amoxicillin
40
Q

when can a child return to school if thye have scarlet fever

A

24 hours after start of ABX tx

41
Q

Diphtheria

  • bacteria?
  • transmission
  • host
  • incubation
  • toxin?
  • can lead to?
  • diagnosis
  • tx
  • prophylaxis for close contacts?
  • prevention
A

Corynebacterium diphtheriae: gram+ rod
transmission=
1. aerosol droplets causes respiratory diphtheria
2. skin contact causes cutaneous diphtheria

Humans are the ONLY HOST

incubation: 2-5 days
* *exotoxin causes the inflammatory response

CM 
RESPIRATORY: 
1. pseudomembranous pharyngitis--- grayish-white membrane that is friable (will bleed if scraped) 
\+sore throat
\+fever 
\+malaise 
\+nasopharyngeal s/s 
2. severe lymphadenopathy--bulls neck

CUTANEOUS:
1. initial papule–>chronic non-heling ulcer

*can lead to systemic toxemia: Myocarditis, arrhythmias, neuronal tissue damage, renal tubular necrosis— all secondary to the exotoxin

diagnosis:
1. throat swab sent for gram stain and culture–>gram+ rods with blue and red metachromatic granules
2. Positive Elek test for toxin

TX:
1. Diphtheria antitoxin immunoglobulin (horse serum)—GIVEN PROMPTLY— most important***
DO NOT WAIT FOR CULTURES TO COME BACK—GIVE ANTITOXIN IMMEDIATELY

  1. Erythromycin IV or PCN IM x2 weeks–switched to PO when PT can tolerate
  2. PT needs to be placed in isolation room
  3. cardiac monitoring
PREVENTION: 
1. DTaP sched: 5 doses given at 
2MO
4MO
6 MO
b/w 15-18MO 
b/w 4-6 Yrs

Tdap booster:
11-12 YO
pregnant mothers and those around them
10 year intervals after 11-22 yrs of age OR after any major injury if the last booster was 5 yrs ago or longer

42
Q

DTaP vs Tdap

A

DTap= combo of diphtheria, tetanus and pertussis vaccine

Tdap= booster for the same three– lower dose vs the initial vaccine

43
Q

when can a diphtheria PT come off respiratory isolation

A

until 2 consecutive cultures 24 hours apart are negative

44
Q

Tetanus

  • bactiera?
  • CM
  • MC initial symp adult and neonate?
  • transmission—MC infection site in adults?
  • diagnosis
A
  • *Clostridium tetani: gram+ rod anaerobe spore forming
  • *produces a powerful NEUROTOXIN: tetanospasmin–blocks neuron inhibition by blocking release of inhibitory GABA and glycine—causing severe muscle spasms

**completely preventable with vaccine

Transmission:

  • 20-30% of adult cases have no visible wound
  • superficial abrasions to the limbs are the MC infection sites in adults

CM:
1. MC initial symp= trismuss
2. muscle pain and stiffness
3. back pain–opisthotonos—- arched back
4. aphagia
NEONATES: diff feeding is the usual presentation

Diagnosis:

  • **clinical
  • can also do cultures or serum tests

TX:

  1. entry wound should be ID, cleaned and debrided of necrotic material
  2. IM Human tetanus immune globulin (TIG) EARLY ON
  3. Metronidazole DOC—alterntive is PCN
  4. Benzos like Diazepam for spasms
  5. IV mag has been shown to improve muscle spasm
  6. airway protection

Prevention:

  1. DtaP vaccine
    * 2MO
    * 4MO
    * 6MO
    * b/w 15-18 MO
    * b/w 4-6 TO
  2. Tdap booster
    * 11-12 YO
    * then every 10 yrs
45
Q

what does a PT get if they never had any vaccination for tetanus

A
  • 1 dose Tdap (First dose should always be Tdap)
  • followed by 2nd dose Td or Tdap 4 wks later
  • 3rd dose Td or Tdap 6-12 MO after 2nd dose

then every 10 yrs get the tDap

46
Q

Td vs DT

A

Td= diphtheria and tetanus toxoid

DT= diphtheria and tetanus vaccine

47
Q

Botullism

  • bacteria?
  • transmission for adults, infants
  • CM adults and infants
  • diagnosis
A

Clostridium botulinum–anaerobic, gram+ spore forming
Produces a NEUROTOXIN—inhibits ACH release at NMJ—weakness, flaccid paralyss and respiratory arrest

Transmission:
adult: ingestio of preformed toxin in canned, smoked and vacuum packed foods

infant: honey ingestion
wound: very rare—-IVDU

CM:

  1. symmetric cranial nerve palsies
  2. descending flaccid paralysis of voluntary muscles —starts proximal muscles weakness—progresses distally
  3. Cranial neuropathies: four D’s
    * diplopia
    * dysarthria–muscles for speech are weak/paralyzed
    * Dysphonia
    * dysphagia
  4. dilated fixed pupils
  5. dry mouth
  6. GI s/s
  7. ptosis
  8. ophthalmoplegia
  9. facial paralysis
  10. impaired gag reflex

INFANTS: floppy baby syndrome, lethargy, weakness, feeding difficulties, hypotonia,* weak cry*

Diagnosis:
***clinical

TX:

  1. Antitoxin first line tx
    * if >1 YO: equine-derived heptavalent antitoxin
    * if <1 YO: human-derived botulism immune globulin (BIG-IV)
  2. NO ABX for foodborne or infantile ****
  3. YES ABX for wound botulism
48
Q

DtAP goes to?

A

kids

49
Q

Tdap goes to?

A

adults

pregnant

50
Q

what age can parents safely give kids honey

A

at least 12MO

51
Q

why do we not give ABX to foodborne or infantile botulism

A

bc the abx can worsen dz via toxin release from lysis of bacteria

52
Q 
Clostridial Myonecrosis 
also called? 
bacteria? 
-toxin? 
-etioloiges
A

Gas Gangrene

  • LT**
  • traumatic inculation with CLostridium perfringens—anaerobe gram + rod
  • *produces Alpha toxin (Lecithinase)
  • they double in number every 7 minutes**

etiologies:
* crush injuries or penetrating trauma that devitalizes tissue
* this creates an anaerobic envir

CM: very rapid progression

  1. sudden intense pain is FIRST symp
  2. skin changes: red/purple—->black)
  3. tenderness
  4. Bullae formation
  5. crepitus–gas
  6. untreated can lead to bacteremia, hypotension, MOF

Diagnosis:

  • clinical
  • blood cultures
  • obtain Xrays=air in soft tissues, want proximal views tooo

TX

  1. IV ABX– PCN + Clindamycin (metronidazole and tetracycline for PCN allergic OR just clindamycin alone)
  2. emergent surgical debridement
  3. possible amputation
  4. hyperbaric O2 can improve survival
53
Q

Cholera

  • bacteria
  • toxin?
A

Vibrio Cholerae—gram negative rod

transmissino: fecal-oral from conaminated water and food
**shellfish
**shrimps
**oysters
releases ENTEROTOXIN–choleragen

CM:

  1. large volumes of watery diarrhea–rice water stool
  2. dehydration can lead to electrolyte imablances–>cardiac and renal failure
  3. acidosis and hypoK
  4. matter of hours if untx…. can be profoundly dehydrated and die

diagnosis:
- culture of stool

tx:
1. prompt and adequate water and electrolyte replacement
2. ABX: tetracyclines, fluoroquinolones or macrolides not really necessary but shorten the duration of s/s

54
Q

Lyme Dz

  • bacteria
  • incubation pd
  • CM for the stages
  • diagnosis
A

Borrelia burgdofrgeri gram- spirochete
*deer tick–>lxodes scapulris
MC spring and summer

incubation= 3-30 days

CM:
1. early localized/stage 1/ (7-10days) : erythema migrans (90%)–expanding, warm, annular, erythematous rash that has central clearing—bulls eye or target appereance
after tick bite
+/- viral like syndrome–fatigue HA fever malaise arthralgias etc

  1. Early disseminated/stage 2 (1-12 weeks):
    -neurologic: bilateral cranial nerve palsy–CNVII aka facial nerve palsy MC aka bells palsy, HA, meningitis, weakness, neuropathy
    -cardiac: AV block MC, pericarditis, arrhythmias
    -multiple erythema migrans lesions
    “Key LYME pie to the FACE”
    F=acial nerve palsy
    A=arthritis
    C=Cardiac block
    E=erythema migrans
  2. Late dz or stage 3:
    - intermittent or persistent arthritis MC–esp large joints
    - –>knee MC
    - persistent neurological symptoms: subtle cognitive changes, distal paresthesias, spinal radicular pain, subacute encephalitis

Diagnosis:
**mc clinical–esp in early stage with the rash— these PT will be seroNEGATIVE
**serologic testing:
1. ELISA–>if postiive then do a Western Blot for confirmation
2. only done in patients who meeet the following criteria:
A. reside or travel to an endemic area
B. risk factor for tick exposure
C. Symps consistent with early disseminated or late lym dz

55
Q

which stage of the ticks life cycle transmits the dz more often nd why

A

Nymphal stage—they feed in the SUMMER which accounts for the highest rate of dz May-september
size of a poppy seed and bites are rarely noticed**

more so than the larval and adult stages

56
Q

how long does a tick need to feed to transmit infectious “dose”

A

24-48 hours

57
Q

list the states MC for lyme

A

NJ
PA
NY
CT

58
Q

can serologic testing for lyme determine if the infection is acute or past?

A

no

once someone has lyme.. they will show up positive

59
Q

how long does it take for a + to show on serologic testing for lyme

A

weeks

60
Q

what diseaes can cause a false positive serologic test for lyme

A

syphilis
lupus
***other spirochetal dz

61
Q

tx for lyme disease

  1. early disease
  2. late or severe
  3. prophylaxis
    * *prregnant?
A
  1. early dz
    *Doxycycline BID x 10-21 days for early localized
    *Doxycycline BID x 14-28 days for early disseminated
    Amoxicillin and Cefuroxime are alternative
    PREGNANT: Amoxicillin x 14-21 days
    can also use Azithromycin or Erythromycin
  2. Late or severe (heart block, syncope, dyspnea, CP, CNS symps)
    * IV Ceftriaxone
  3. Prophylaxis—given w/in first 72 hours of tick removal if tick present for >36 hours and in endemic area
    * Doxycycline 200mg X1 dose
    * if allergic to doxy or cannot be used, no prophylaxis given

DOXY IS CONTRA IN PREGNANCY

62
Q

what serologic test confirms diagnosis of lyme and when is it done

A

Western Blot Immunoblot assay

**done after a + ELISA test

63
Q

when would you administer lyme dz prophylaxis (3)

A
  1. tick is known lxodes scapularis
  2. tick attached >36 hours
  3. pt in endemic area

must get doxy within 72 hrs of bite

64
Q

tx for early disseminated lyme dz

  • what is the s/s
  • tx?
A

s/s= erythema migrans rash

tx= doxycycline
contra to doxy— give Amoxicillin ** or Cefuroxime

65
Q

tx for facial nerve palsy and/or joint involvement phase of lyme dz

A

tx= doxycycline

contra to doxy— give Amoxicillin ** or Cefuroxime

66
Q

cardiac and neuro manifestations for lyme dz– what is tx

A

IV ceftriaxone

67
Q

reinfection with lyme dz tx?

A

tx= doxycycline

contra to doxy— give Amoxicillin ** or Cefuroxime

68
Q

Rocky Mounted Spotted Fever:

  • bacteria?
  • has affinity for what kind of cells
  • what states
  • vector? SE states? western states?
  • CM
  • diagnosis
  • tx
A

Rickettsia rickettsia–gram neg short rod
obligate intracellular bacteria

affinity for vascular endothelial cells—causes the vascular injury

occurs primarily in South East states—NOT the rocky mountains
Vector in SE States= DOG TICKS… Dermacentor variabilis
Vector in Western US= wood tick…Dermacentor andersoni

Can be fatal is left untx

CM:
1. abrupt onset of HA, fever, chills, malaise, mylagias, arthraligias, N/V, lethargy

  1. 2-6 days later: rash that starts as macules then progresses to pretechiae—rash FIRST appears on PALMS AND WRISTS AND SOLES AND ANKLES–>then moves inward to trunk—basically starts distal and moves inward
  2. as rash progresses it can cause edema, encephalitis, cardiac and bleeding disorders, delirium coma and death

diagnosis:
clinical: fever+ rash + hx of tick exposure
serologies: indirect immunofluorescent antibody test
LABS: thrombocytopenia, pancytopenia, hyponatremia my occur
CSF: low glucose and pleocytosis (incr cell count)
**dont wait for serology to tx**

TX:
Doxycycline DOC
Chloramphenicol is 2nd line and for pregnancy

69
Q 
Gonorrhea 
-bacteria? 
-transmission
*what parts can it infect 
*RF (7) 
CM for men and women...MC? 
CM for DGI 
incubation pd--m and w
A

Neisseria gonorrhoeae
gram -

trans:
* sexually
* newborns can get it from infected mom

Can infect: genital tract, anorectal and pharyngeal

RF

  • new or multiple partners
  • unprotected sex
  • substance abuse
  • low education level
  • low socioeconomic status
  • MSM
  • hx of STI

incbation pd:

men: 2-7 days
women: <10 days

CM for men:

  1. MC is urethritis
  2. mucopurulent/copious urethral discharge
  3. epididymitis
  4. prostatitis
  5. balanitis

CM women:

  1. mucopurulent vaginal discharge
  2. intermestrual bleeding
  3. urethritis
  4. bartholin gland infection
  5. PID
  6. lower abd pain and tenderness
  7. fever
  8. CMT— sign of PID
  9. Adnexal tenderness
  10. Perihepatitis– also called Fitz-Hugh-Curtis Syndrome

CM for Disseminated Gonococcal infections:

  • septic arthritis
  • MCC in Men <30 YO
  • can also go to anorectcal, throat and eyes
  • anus infection= usuall asympto…. but can cause bloody and purulent discahrge
70
Q

Perihepatitis– also called Fitz-Hugh-Curtis Syndrome

  • define
  • s.s
A

occurs in 4% of women with gonorrhea
associ with PID and inflammation of the liver capsule

causes right upper quadrant abdominal pain, fever, nausea, and vomiting, often mimicking biliary or hepatic disease

71
Q

Diagnosis for Gonorrhea

A

Nucleic acid amplification tests–NAATS via urine or vaginal swab

gram staining—- >90% urethral sample from men and 50% for endocervical sample from W

72
Q

Tx for gonorrhea

tx for gonococcal arthritis

A

Gonorrhea:

  1. Ceftriaxone 250 mg IM**** and Azithromycin 1gram PO once
  2. if suspected PID: ceftriaxone + doxycycline x1 week
  3. Partner is tx as well

Disseminated gonococcal infection:
1. IV Ceftriaxone

**condoms MAY limit transmissino

73
Q

Syphilis

  • bacteria?
  • transmission
  • CM
A

Treponema pallidum
gram - spirochete VERY SLOW GROWING

transmission:
- sex
- pregnant women to fetus

CM: three phases bc it is muli-stage dz

  • can present at any stage
  • sometimes not show s/s for years
  1. PRIMARY
    * chancre= PAINLESS ulcer w/ raised indurated edges
    * heals spontaneoulsy within 3-4 weeks
    * nontender regional lymphadenopathy near chancre lasting 3-4 weeks
  2. Secondary Syphilis “great imitator”
    * s/s occur few weeks-6MO
    * maculopapular rash= diffuse bilaterally +soles +palms
    * Condyloma lata= wart like, moist lesions involving mucous membranes and other moist areas–VERY contagious
    * constitutional symps= fever, maliase, HA, wt loss, lymphadenopathy, alopecia

about 1/3 of primary and secondary syphilis will resolve on their own w.o tx***

  1. Tertiary or late syphilis
    * may occur 1-20 years after initial or secondary infection
    * Gumma= noncancerous granulomas on skim and body tissues
    * Neurosyphilis= HA, meningitis, dementia, vision/hearing loss, Tabes Dorsalis (demyelination of posterior spinal columns) leads to ataxia, areflexia, “lightening like” burning pain and weakness
    * Argyl-Robertson pupil= small irreg. pupil that constricts with accomidation but is NOT reactive to light
    * cardiovascular= aoritis, aortic regurg, aortic aneurysms
74
Q

Tabes Dorsalis

A

demyelination of posterior spinal columns) leads to ataxia, areflexia, “lightening like” burning pain and weakness

**teritary syphilis

75
Q

gumma

A

noncancerous granulomas on skim and body tissues

**tertiary syphilis

76
Q

Argyl-Robertson pupil

A

small irreg. pupil that constricts with accomidation but is NOT reactive to light

77
Q

screening for syphilis

-false positives occur frm what dz?

A
  1. rapid plasma reagin (RPR)
  2. venereal disese research laboratory (VDRL)
    * *these tests looks for titers to non-treponemal antigens

results are + in most cases of primary syphilis
***false + can occur bc does not test for treponemal antigens…. in dz like: leprosy, hep B, EBV, autoimmune dz

78
Q

confirmatory testing for syphilis

A
  1. Fluorescent treponemal antibody absoprtion (FTA-ABS) ***specific for Treponema pallidum antibodies
    remain positive for life–even after effective treatment

**more expensive and difficult to perform vs the screening tests

  1. Darkfield microscopy–direct visualization
79
Q

tx for syphilis

A

PCN is DOC for all stages

  1. primary, secondary or early latent
    * **PCN G Benzathine IM one dose
    * *PCN allergic: Doxycycline (PO) or ceftriaxone (IM/IV)
  2. Late
    * **PCN G Benzathine IM once weekly x3 weeks
  3. neurosyphilis
    * **IV PCN G potassium x10-14 days
80
Q

which can be given IV

PCN G BEnzathine or PCN G Potassium

A

potassium

Benzathine will cause cardiac arrest

81
Q

Jarish-Herxheimer rxn

A

acute self limiting febrile rxn

occurs within first 24 hours after receiving therapy for a spirochetal infection (syphilis, lyme dz)

82
Q

chlamydia

  • bacteria
  • what else can the bacteria cause
  • CM–women, men, newborns
  • diagnosis
  • tx
A

Chlamydia trachomatis–very small, intracellular obligate
*causes: conjunctivitis, genital tract infections (urethritis, lymphogranuloma venreme)

PTs infected with this bacteria co-infected with N. gonorrhoeae in 10-30% of cases

CM: almsot 1/2 cases are asympto **
Women: cervicitis, urethritis, salpingitis, PID
Men: urethritis, epidimyitis, procitis
*conjuncivitis can occur via touching gentiles then eyes or in newborns
*reactive arthritis–>arthritis, urethritis, and uveitis=triad MC in men—THIS IS NOT SEPTIC ARTHRITIS
*Fitz-Hugh curtis syndrome: perihepatits… MC with this vs gonorrhea

Newborns: Ophthalmia neonatorm

Diagnosis:
-nucleic acid amplification tests NAATs–urine or vag swab

TX
1. Azithromycin 1gm PO
OR
Doxycycline 100mg BID x10 days
2. partner is tx too— no sex for 7 days after taking meds
3. high risk PT–consider gonorrhea tx too

83
Q

what are the three types of Chlamydia bacteria

A
  1. Chlamydia trachomatis (STD)
  2. Chlamydia psittaci (parrots)
  3. Chlamydia pneumoniae
84
Q

watery, mucopurulent discharge with pruritis and dysuria

A

urethritis

85
Q

Ophthalmia neonatorum

  • etiologies?
  • whch is most visually threatening and which is MC?
A

Chlamydia trichomatis and Neisseira Gonorrhea

Gonorrhea is Most visualy threatening but chlamydia is MC

86
Q

septic arthritis vs reactive arthritis

A

septic arthrits– occurs with gonorrhea infection

Reactive arthritis– occurs with chalymida and has the triad of

  • arthralgia
  • uveitis
  • urethritis
  • cant see cant pee cant climb a tree*
  • this is also auto-immune related
87
Q

what states is the expedited partner therapy for chlamydia not allowed

A

kentucky
west virginia
south caroline

88
Q

Lymphogranuloma Venereum (LGV)

  • bacteria
  • MC seen where
  • CM
  • diagnosis
  • tx
A

caused by Chlamydia trichomatis L1-L3 immunotypes

MC seen in tropical and subtropical areas of world

CM:

  1. painless genital ulcer at the site of inoculation
  2. second phase appears 2-6 wks later–painful inguinal and/or femoral lymphadenopathy

diagnosis is clinical

tx: doxy bid 100 mg x 21days

89
Q

Trichomoniasis

  • organism?
  • transmission
  • CM
  • diagnosis—best test?
A

PROTOZOA—trichomonas vaginalis

transmission: sexual contact
primarly located in vagina and prostate

***most prevalent nonviral STI in US

CM
1. women can have malodorous, frothy yellow/green vaginal discharge
2. vaginal itching
3. dysuria
4. cervical petechiae–strawberry cervix
MEN ARE USUALLY ASYMPTO

Diagnosis: NAAT (best test) OR saline wet mount—will see flagellated protozans
**vaginal PH is very alkaline

TX:

  1. Metronidazole 2g PO once OR 500mg BID x7 days (best this route if recurrent)
  2. partner needs to be tx
  3. condoms MAY limit transmission

Clin Med (52 decks)

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