Common bacterial infections Flashcards

1
Q

What is the cause of diphtheria?

A

CH 187: DIPHTHERIA
- By Corynebacterium diphtheria – aerobic gram(+)
bacilli
- Acute, contagious
Epid:Transmission
- skin transmission via airborne respiratory droplets (3
feet)
- direct contact with respiratory secretions, exudate
from skin lesion
- impt: asymptomatic respiratory tract carriage
- can remain in dust/fomites x 6mos
- CD exclusive inhalant of human mucus membranes
- Humans are the only known reservoir (exclusively in
skin and mucosa)
IP: 1-5 d

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2
Q

How is diphtheria transmitted?

A

Transmission
- skin transmission via airborne respiratory droplets (3
feet)
- direct contact with respiratory secretions, exudate
from skin lesion
- impt: asymptomatic respiratory tract carriage
- can remain in dust/fomites x 6mos

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3
Q

What is the pathophysiology of diphtheria?

A

Patho
- non-invasive organism
- remains in the superficial layers of skin/respiratory
mucosa inducing local inflammation
- lysogenic CD bacteriophage encodes exotoxin which
inhibits protein synthesis causing local tissue necrosis
- local signs of inflammation
- infection of pharynxà form dense, necrotic coagulum
(organism + RBC + WBC + epithelial cells + fibrin) –>
becomes gray, brown, leatherlike adherent
pseudomembrane
a. difficult to remove
b. reveals bleeding edematous submucosa –>
suffocation of aspirated membrane
c. Bull neck appearance –> intense soft tissue
edema and cervical adenitis (children with
small airway)
- Fatality due to airway compromise and toxin mediated
complications

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4
Q

What are the clinical manifestations of diphtheria?

A

CM:
1. Respiratory diphtheria (94%)
- Facial & pharyngeal (most common), laryngeal &
tracheobronchial
- Nose: shallow ulceration of external nares & upper lip
is characteristic
- Abrupt LG fever (rarely above 39C), sore throat, dev’t
of membrane (extend widely) à pharynx and
tracheobronchial tree, bull neck appearance
2. Cutaneous (10%)
- Superficial nonhealing ulcer, ecthymic with gray-brown
membrane (tender, erythema, and with exudate)
- Usually extremities
- Heals in 2-3 mos, w/ a scar
3. Systemic – cause 50-60% of deaths
a. Cardiac
- Myocarditis in 2/3s of pxs
- Occurs in 2nd-3rd week of infection
- Dysrhythmia, Vtach, HF
- The first sign of cardiac involvement is tachycardia
disproportionate to the degree of fever
b. Neurologic
- First few days
- Cranial neuropathies characteristically occur in the 6th
week: strabismus, BOV
- Local paralysis of the soft palate and posterior pharynx
à regurgitation of swallowed fluids
- Symmetric polyneuropathy: distal muscle weakness
with proximal progression
- 1st signs: Dysphagia and nasal speech
c. Others: otitis externa, conjunctivitis,
arthritis
- Recovery from myocarditis and neuritis usually slow
but complete

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5
Q

How is diphtheria diagnosed?

A

Dx
1. CBC - moderate leukocytosis
2. Throat swab membrane GS & C/S – specimen should
be collected beneath the membrane including the
membrane itself
- Repeat cultures of nose and throat 2x (24h apart) after
completion of tx to ensure eradication of org
3. Baseline ECG – detect myocarditis ASAP
- Repeat 2x/week for 4-6 weeks
- ST-T wave changes, variable heart block, dysrhythmia
4. Serum Troponin I – correlate with severity of
myocarditis
5. Soft tissue neck XR/CT/UTZ – prevertebral soft tissue
swelling, enlarged epiglottis, narrowing of subglottic
region
6. 2D echo – demonstrate valvular vegetations

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6
Q

How is diphtheria managed?

A

Mgt
1. Neutralization of free loosely bound toxin with
diphtheria antitoxin (DAT)
- 40K-60K U <2d of sx
- 80K-120K U >2 d of Sx
2. Eradication of the organism
- Pen G 100,000-150000 U/k/d q6h x 10d
- Erythromycin 40-45 mkd q6h x 14d
3. Supportive – IV hydration, intubation (MV,
tracheostomy), bed rest
4. Complete immunization (convalescent) – protection
lasts 10 yrs
- Vax does not eliminate carriage of CD in the pharynx,
nose or skin
- Infection does not confer immunity
- Only effective way of preventing cases and outbreaks
- If unimmunized à complete vaccination
a. 6wk-6yo: DTaP (5)
b. >6yo: Tdap-Td-Td
c. 11-12 yo: Tdap q10y
5. Carriers – sx free but with CD in nasopharynx
- Erythromycin 40-45 mkd q6h x 7d
- Benzathine penicillin (<30kg) 600,000 U IM single dose;
(>30kg) 1.2M U IM single dose
- F/u after 2 weeks & if carrier state persists, give
additional 10d course of erythromycin and consider
tonsillectomy/adenoidectomy
6. Patient contact – household and hospital contact
(unimmunized or partially immunized)
- Nasopharyngeal GS/CS
- Erythromycin 40-45mkd qid x 7d
- Benzathine penicillin (<30kg) 600,000 U IM single dose;
(>30kg) 1.2M U IM single dose
7. Infection control – strict isolation precaution for the
duration of tx (10d)
- Droplet precautions
- Vaccinate all hospital workers

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7
Q

Acute spastic paralysis

A

Tetanus

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8
Q

What is the etiology of tetanus?

A

Etiology:
- Clostridium tetani
- Anaerobic gram (+)
IP: 2-14d, but may occur months after an injury

Acute spastic paralysis
- Favorable prognosis: long incubation period, absence
of fever, localized disease
- Unfavorable prognosis: onset of trismus <7d afer
injury, generalized tetanic spasms occurring <3d after
onset of trismus, cephalic tetanus

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9
Q

How is tetanus transmitted?

A

Transmission
- Associated with traumatic injury (penetrating wound
from a dirty object
- Introduced spores germinate, and produce tetanus
toxin

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10
Q

What is the pathophysiology of tetanus?

A

Patho:
Traumatic injury –> bacterial spores enter injury –> spores
converted to vegetative forms w/c produce tetanospasmin –>
blood/LN dissemination –>
- SC & brain: binds to NMJ (retrograde axonal transport)
à GABA inhibition –> blocks inhibition of antagonistic
muscles –> spasmic paralysis
- ANS: Ach inhibition –> autonomic dysfunction
- Note: vs botulism: Ach inhibition –> flaccid paralysis

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11
Q

What are the clinical manifestations of tetanus?

A

CM
3 main components: muscle rigidity, muscle spasm & autonomic
dysfunction
1. Neonatal or umbilical tetanus – most common form
- Occurs within 3-12d of birth
- Progressive difficulty in feeding to jaw stiffness
- Generalized weakness
- Hunger, crying, paralysis, stiffness and rigidity to touch,
spasms, opisthotonos
- Cyanosis or pallor, apneic episodes
- unsterile umbilical cord stump, unsanitary delivery of
baby, mom incomplete immunization hx
- constipation and urinary retention
2. Generalized tetanus
- Most common presentation
- Tetanic paralysis usually more severe in the 1st week,
stabilizes in the 2nd week, then ameliorates gradually in
the next 1-4 wks
- Progressive stiffness of voluntary ms:
a. Trismus: masseter muscle spasm or lockjaw
b. Risus sardonicus: orbicularis oris, sardonic
smile of tetanus
c. Opisthotonos: neck and back; arched
posture of extreme hyperextension
d. Board-like abdomen: trunk
e. Flexed arms and extended legs: extremities
- Laryngeal & respiratory muscle spasm can lead to
Headache, restlessness, irritability, fever, followed by
stiffness, difficulty chewing, dysphagia, neck muscle
spasm
- Accumulation of secretions because of inability to
swallow
- Intact sensorium, severe pain during each spasm
- Fever: usually absent, if present HG due to energy
generated from tetanic spasm
- Seizures: sudden tonic contractions of the muscles
- Smallest disturbance by sight, sound, or touch may
trigger a tetanic spasm
a. May be so violent to cause upper airway
obstruction and vertebral fractures
- Dysuria and urinary retention from bladder sphincter
spasm
- Hyperactive DTR
- Sympathetic overactivity (SOA): Autonomic sx: resting
tachycardia, arrhythmia, labile hypertension, sweating,
depression of bowel motility and bladder dysfunction
a. Occurs a few days after onset of spasms
3. Localized tetanus
- Chronic form, prodrome of gen tetanus
- May reflect partial immunity to tetanospasmin
- Painful spasms of muscles adjacent to wound site
- May precede generalized tetanus
a. Cephalic tetanus: rare form
b. Involve bulbar musculature. Results in
retracted eyelids, deviated gaze, trismus,
risus sardonicus, spastic paralysis of tongue
and pharyngeal membrane
c. Affecting muscles innervation CN 3,4,7,9,10
d. Follows head injury, OM, FB in nose

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12
Q

What are the diagnostics for tetanus?

A

Dx
1. CBC – usually N, or mod leukocytosis
2. RBS, Na, K, Cl, Ca, Mg - r/o abN
3. CXR – r/o aspiration PN
4. BUN, Crea, CSF, septic workup (neonates), ABG, 12L
ECG
5. wound d/c GS/CS – not indicated because only (+) in
30%. Does not indicate whether organism contains
toxin
6. CSF/ lumbar puncture – not nec. Usu N or only inc
opening pressure
7. Elev CK, aldolase
8. Spatula test – using a spatula/tongue depressor, touch
oropharynx eliciting reflex spasm of masseters and bite
the spatula (+ result)
9. EMG – continuous discharge of motor subunits and
absence of the silent interval normally observed after
an action potential

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13
Q

Scoring system for Neonatal tetanus

A
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14
Q

Staging system for non-neonatal generalized tetanus

A
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15
Q

Ablett Classification of severity of tetanus

A
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16
Q

Management of tetanus

A
  1. neutralization of circulating/unbound toxin: TIG 250U
    or ATS 1500-3000IU, ideally HTIG 500U IM
    a. If TIG unavailable: human IVIG, equine, or
    bovine-derived tetanus antitoxin
    b. Upon d/c, tetanus toxoid
  2. Active Vaccination
    DTaP, DTwP, Tdap, Td
  3. Elimination of exotoxin production
    e. Wound care: Wound excision &
    debridement
    a. Abx
    i. Metronidazole po/iv 30mkd x
    10d – DOC
    ii. Pen G x 10d
    Neonates 100K U/k/d q12
    Children 100L U/k/d q6
    Adult 5M q6
    iii. Alt for allergy: erythromycin,
    tetracycline
  4. Prevention and control of spasms:
    a. For generalized tetanus: muscle relaxants
    and NM blockers (Pancuronium,
    vecuronium)
    b. BZDs, MgSO4
    c. Control of sz (Pb)
  5. Severe: Intubation to prevent aspiration, early
    tracheostomy
  6. Control of autonomic dysfuntion – MgSO4 to suppress
    cathecholamine release
  7. Quiet, dark, secluded setting
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17
Q

How is tetanus prevented?

A

Prevention
1. Vaccination with DTaP, Tdap, Td
2. Pregnant women: 1 dose Tdap during each pregnancy,
at 27-36 weeks AOG
3. Tetanus prophylaxis in wound mgt
a. Clean minor wounds and <3doses of Td:
Tdap or Td
b. Clean minor wounds and >3 dose of Td
within the past 10 yrs: no need for toxoid
c. All other wounds and <3 doses of Td: Tdap
or Td and TIG
d. All other wounds and > 3 dose of Td within
the past 5 years: no need for toxoid/TIG

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18
Q

What is botulism and its cause?

A
  • Acute, flaccid, paralysis
  • Gram (+), spore-forming, obligate anaerobe whose
    natural habitat is soil, dust, and marine sediments
  • Strains endure sev hrs of boiling, survive food
    preservation; but the toxin is heat labile at >85C for
    5min (canned foods)
  • Botulinum toxin is the most poisonous substance
    known, lethal dose = 10-6 mg/kg
  • Most striking epidemiologic fx is its age of distribution
    = 95% cases infants between 3wks to 6mos age, peak
    2-4 mos
  • Risk factors: breastfeeding, ingestion of honey, slow
    intestinal transit time (<1 stool/d), contaminated water
  • Represents a medical and public health emergency
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19
Q

What is the pathophysiology of botulism?

A

Patho
- Toxin blocks NM transmission and causes death
through airway and respiratory muscle paralysis
- Botulinum toxin is carried by the bloodstream to
peripheral cholinergic synapses, where it binds
irreversibly, blocking acetylcholine release, and causing
impaired NM and autonomic transmission

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20
Q

How is botulism transmitted?

A

Transmission
Infant botulism – ingestion of spores
Foodborne botulism – ingestion of preformed botulinum toxin
contained in improperly preserved or inadequately cooked food
Wound botulism – spore germination from traumatized tissue
Inhalational botulism – aerosolized botulinum toxin is inhaled

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21
Q

What is the classic triad of botulism? What are the clinical manifestations?

A
  1. Classic triad
    a. Acute onset of symmetric flaccid
    descending paralysis with clear sensorium
    b. No fever
    c. No paresthesia
  2. Symmetric, descending, flaccid paralysis – beginning in
    the CN musculature. Multiple bulbar palsies.
  3. Infant botulism
    - poor feeding, weak suck, feeble cry, drooling,
    obstructive apnea
    - generalized weakness and hypotonia, diminished
    spontaneous movt
    - loss of head control is a prominent sign
    - first sx may be dec freq or absence of defecation
    - respiratory arrest from sudden airway occlusion by
    unswallowed secretions or obstructive flaccid
    pharyngeal musculature
  4. Food-borne/ wound botulism
    - Onset of neuro sx follows a characteristic pattern of
    diplopia, BOV, ptosis, dry mouth, dysphagia,
    dysphonia, dysarthria, dec gag and corneal reflex
    - Toxic acts only on the motor nerves
    - No paresthesia
    - Nausea, vomiting, diarrhea
    - Constipation once flaccid paralysis is evident
    - Begins 12-36h after ingestion of food (range 2h-8d)
    - Fever in wound botulism
  5. Inhalational botulism
  6. Mild (min ptosis, flattened facial expression, minor
    dysphagia, dysphonia) to fulminant (rapid extensive
    paralysis, frank apnea, fixed, dilated pupils)
  7. Fatigability with repetitive muscle activity – clinical
    hallmark of botulism
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22
Q

How is botulism diagnosed?

A

Dx
1. Botulinum toxin – serum, wound, enema fluid, feces
2. EMG – distinctive finding: facilitation (potentiation) of
the evoked muscle action potential at high frequency
(50 Hz) stimulation
- Infant: BSAP (brief, abundant, motor unit action
potentials) is characteristic
- N nerve conduction velocity and sensory nerve fxn
3. CBC, BCS, CRP – r/o sepsis

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23
Q

how is botulism managed?

A

Mgt
1. Human botulism IG IV (BIG-IV) 50-100 mg/kg SD – given
ASAP
- Shortens mean hospital stay from 6wks to 2 wks
2. Equine heptavalent (A-G) botulism antitoxin – for older
pxs
3. Abx – not part of tx of uncomplicated infant/foodborne
botulism
- Reserved for tx of secondary infections, absence of
antitoxin tx
- DOC: TMP-SMX 20mkd IV q6/8
- Avoid aminoglycosides because may potentiate the
blocking action of botulinum toxin at the NMJ
4. Proper positioning
- Supine on rigid-bottomed crib/bed, head titled at 30
degrees. Small cloth roll under the cervical vertebrae
to tilt the head back so the secretions drain to the
posterior pharynx and away from the airway and
improve respiration
. Prophylactic ET intubation – indications: diminished
gag and cough reflex and progressive airway
obstruction by secretions
6. NGT feeding until sufficient oropharyngeal strength
and coordination enable BF/bottle feeding – EBM is
most desirable food
7. Hydration
8. Stool softeners (lactulose) – mitigate constipation

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24
Q

What are the complications of botulism? Prognosis?

A

Complic
1. Nosocomial infections
2. PN, UTI, OM
3. strabismus

Prognosis
- full and complete recovery (~4wks).

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25
How is botulism prevented?
Prevention - Avoiding suspicious foods (canned foods improperly preserved) - Heat all canned foods to 85C for >5min - Avoid honey until 1 yo - Continue BF
26
What is Staphylococcus aureus? How is it transmitted?
- Gram (+) aerobic bacteria, coagulase (+) - Most common cause of pyogenic infections of the skin and soft tissues Transmission: Autoinoculation or direct contact
27
What are the clinical manifestations of staph aureus? How is it diagnosed?
CM: 1. Osteomyelitis, suppurative arthritis, abscesses, pyomyositis, empyema, IE 2. Toxin-mediated: food poisoning, scalded skin syndrome, toxic shock syndrome 3. Pyogenic skin infections: impetigo, ecthyma, cellulitis, necrotizing fasciitis 4. Sepsis 5. Respi: tracheitis, PNA (empyema, pneumatoceles) 6. Renal abscesses 7. Acute endocarditis of native valves 8. Meningitis Dx: 1. CBC 2. C/S of focus/blood
28
How is S. aureus infection managed?
Mgt: 1. Abscess: I&D 2. Abx: MSSA: Oxacillin 100-200 mkd IV q4/6 co-amox 20-40 mkd q8/12 po/IV MRSA: vancomycin 40-45 mkd IV q6/8 Clindamycin 30mkd IV/po q6/8
29
How is Neisseria gonorrhea transmitted?
Transmission: - Sexual contact or perinatal (via contact with cervical canal during delivery or with contaminated amniotic fluid) - Intracellular diplococcus - Often with co-infection with Chlamydia
30
What is the pathophysiology of gonorrhea?
Patho - Infects primarily columnar epithelium à local inflammatory response that produces a purulent exudate consisting of PMN leukocytes, serum, and desquamated epithelium à endotoxin is cytotoxic causing ciliostasis and sloughing of ciliated epithelial cells
31
What are the clinical manifestations of gonorrhea?
CM 1. Asx’c (80% F, 10% M) 2. Uncomplicated: purulent exudate (urethritis cervicitis, vulvovaginitis, ophthalmitis) 3. Disseminated gonococcal infection (DGI): polyarthralgia + fever + pustular lesions - From hematogenous dissemination - Sx begin 7-30d after infection, within 7d of mens - Asymmetric arthralgia, petechial or pustular acral skin lesions, tenosynovitis, suppurative arthritis - Most common initial sx is acute onset polyarthralgia with fever - Painful, discrete, 1-20mm pink/red macules that progress to MP, vesicular, bullous, pustular, or petechial lesions. Typical necrotic pustule on an erythematous base distributed unevenly over the ext (incl palmar and plantar surface) spacing face and scalp. - 2 clinical syndromes: a. Tenosynovitis-dermatitis syndrome: F, chills, skin lesions, polyarthralgia (wrists, hands, fingers). Synovial fluid Cx (-) b. Suppurative arthritis syndrome: monoarticular arthritis (knee) 4. Neonatal infections: Ophthalmia neonatorum: 2-5d after birth 5. Gonococcal arthritis 6. Amniotic fluid syndrome: PROM, inflammation of placenta and umbilical cord 7. Sepsis and meningitis 8. Scalp abscess 9. Pelvic inflammatory disease (PID) – ascending infection from the urogenital tract causing urethritis, epididymitis (M), edometritis, salphingitis, peritonitis (F) - Fitz-Hugh-Curtis syndrome: dissemination to fallopian tube through peritoneum to the liver capsule
32
how is gonorrhea diagnosed?
Dx 1. DischargeGS/CS – any exudate, eye discharge, nasopharynx, OGT, anorectal area, blood 2. Lumbar puncture with spinal fluid studies 3. C/S for concomitant Chlamydia 4. CBC – elev WBC 5. Nucleic acid amplification test (NAAT) – Sn and Sp
33
What is the management of gonorrhea?
Mgt: 1. Nondisseminated infection, ophthalmia neonatorum: ceftriaxone 250mg IM single dose or cefotaxime 100-200mkd IV q6/8 or Cefixime 400mg po single dose or Single dose cephalosporin IM Plus Azithromycin 1g po SD or doxycycline 100mg po BIDx7d Ceftriaxone remains the empiric abx for gonococcal infections 2. Arthritis and septicemia: ceftriaxone, cefotaxime x7d 3. Meningitis: ceftriaxone or cefotaxime x 10-14d 4. All infants: contact isolation until effective IV abx x 24h
34
What is Shigellosis? How is it transmitted?
CH 199: SHIGELLOSIS - Dysentery - Acute invasive enteric infection - Ingestion of contaminated water or food - Most common in 2-3 yo Transmission: - Person to person (fecal-oral route) - Requires very small inocula to cause illness IP: 12h-7d
35
What is the pathophysiology of Shigellosis?
Patho - Bacteria invade intestinal epithelium through M cells causing death and sloughing of invaded epithelial cells and potent inflammatory response - Shiga toxin is a potent exotoxin that inhibits protein synthesis --> injure vascular endothelial cells --> HUS
36
What are the clinical manifestations of Shigellosis?
CM: 1. HG fever + severe abdominal pain + painful defecation (tenesmus) 2. Diarrhea: watery large volume à small frequent volume, bloody, mucoid stool 3. Abdominal distention, tender rectum, HABS, emesis, anorexia, generalized toxicity 4. CNS (40%): seizure – most common extraintestinal manifestation 5. Dehydration – most common complication
37
How is Shigellosis diagnosed?
Dx: 1. Stool exam: >50-100 PMNs/hpf, fecal blood (presumptive dx), leukocytosis 2. Stool C/S: gold standard 3. BCS: very young, malnourished 4. CBC: inconsistent WBC, shift to the left (inc bands), leukopenia or leukemoid reactions. HUS shows anemia and thrombocytopenia
38
What is the treatment of shigellosis?
Tx: 1. Ciprofloxacin 25mkd BID x 3d – for bloody diarrhea 2. Ceftriaxone 100mkd x 5d 3. Cefixime 8mkd OD po 4. Azithromycin 10mkd po x 3d 5. Increasing resistance to fluoroquinolones
39
How is E. coli transmitted?
Transmission - Person to person - Fecal-oral route (contaminated food & water) IP: 10h to 6d Communicability: as long as the person excretes the bacteria (1-4 wks)
40
What is the pathophysiology of E. coli?
Patho - After ingesting E.coli 0157:H7, the bacteria bind to the intestinal mucosa and release Shiga toxin --> disrupt protein synthesis in the epithelial cells lining the intestinal mucosa --> cell death, mucosal sloughing, bloody diarrhea
41
What are the clinical manifestations?
ETEC: most common cause of traveler's diarrhea patho: adherence factors; heat-labile and heat stable enetrotoxins watery diarrhea manifestations: abdominal pain, nausea, vomiting, little or no fever; usually self-limited EIEC: >1yr old patho: adherence; invasion and inflammation of large intestine diarrhea: watery diarrhea or dysentery manifestations: fever, systemic toxicity, crampy abdominal pain, *tenesmus, often with positive leukocytes EPEC: <2yrs old patho: adherence; effacement of intestines watery, nonbloody diarrhea with mucus vomiting and low grade fever EHEC or Shiga-toxin-producing or verotoxin producing E.coli 6mos-10yrs old; elderly; poorly cooked hamburger is a common cause of outbreaks patho: shiga-toxin production, large bowel attachement; E.coli 0157:H7 is the most virulent serotype and most frequently associated with HUS Diarrhea: initially watery but becomes bloody Fever is not commonly present; 5-10% develop systemic complications such as HUS Enteroaggressive E. coli (EAEC) <2yo; HIV patients, travelers patho: small and large intestine adherence; enterotoxin and cytotoxin production diarrhea: watery, mucoid diarrhea; some patients may have bloody stools low grade fever; little to no vomiting Diffusely adherent (DAEC) >1yr old; travelers patho: adherence factors; toxin production diarrhea: watery abdominal pain and fever
42
How is E.coli diagnosed?
Dx: 1. Serotype O157:H7 – isolation of E.coli that fails to ferment sorbitol on McConkey sorbitol medium 2. Tissue C/S 3. CBC – leukocytosis with left shift 4. Stool exam – leukocyte (+) with EIEC 5. FOBT – (+) in some strains
43
How is E.coli managed and prevented?
Mgt: 1. Supportive – fluid and electrolyte tx 2. Early refeeding: with 6-8h from starting rehydration 3. Antimicrobials – not given for STEC or EHEC due to inc risk of HUS - For ETEC, EPEC, severe watery diarrhea – cotrimoxazole 8-12mkd IV/po q12 For resistant strains: Ciprofloxacin 20-30mkd q12 po/IV Azithromycin 10mkd po x 3d 4. zinc supplements – for malnourished children prevention 1. proper food and water handling, handwashing
44
What are the diseases caused by treponema pallidum?
- Syphilis - Spirochete
45
How are treponema pallidum transmitted?
Transmission: - Vertical via transplacental or SVD - Sexual contact Patho - Bacteria rapidly penetrates intact mucus membranes/abrasions --> primary lesion --> CNS -->What delayed type hypersensitivity in tertiary syphillis
46
What are the clinical manifestations of treponema pallidum?
CM: 1. Primary syphilis (4-6 wks) - Painless chancre: ulcer with raised border at entry site (genital area) + regional lymphadenitis - Firm, round, small - Highly infectious - 10-90d after infection - Heals spontaneously with thin scar (3-6 wks) 2. Secondary - Highly infectious - Syphilitic roseola: few weeks after the chancre heals a. Nonpruritic maculopapular rash in palms and soles b. Wart-like growth c. Heals spontaneously (2-6wks to 12wks) - If untreated: spirochetenemia - Condyloma lata: wart-like plaques in anus or vagina, axilla, groin, buccal mucosa - Mucus patches 3. Latency stage - Infected person is asx’c but continues to have the infection a. Early latent stage - Potentially infectious - Seroreactive w/in 1 year of infection - No sx b. Late latent stage § Not infectious § Seroreactive more than 1 yr after infection § No sx 4. Tertiary/late - Not infectious - Gumma: skin and musculoskeletal - Internal organs - Plus neurologic (neurosyphilis) and CV - Paralysis, numbness, blindness, dementia, death 5. Congenital syphilis - Vertical transmission 100% - Transmission to fetus: as early as 9wks aog - The longer the interval between infection and pregnancy, the more benign the outcome in the infant - Asymptomatic to fatal - Early: 1st 2 yrs a. abortion, stillbirth, hydrops b. osteochondritis, periostitis c. Mucocutaneous rash: erythematous, MP or vesiculobullous followed by desquamation of hands and feet, mucous patches (white plaques) d. Condylomatous lesions e. persistent rhinitis (snuffles) f. Pseudoparalysis of Parrot – painful osteochondritis, refusal to move affected limb g. Congenital neurosyphilis: encephalitis h. Consumptive coagulopathy: thrombocytopenia, splenomegaly i. MOF: hepatosplenomegaly, jaundice, elev LFT, Coomb’s negative hemolytic anemia j. Renal: nephritis, nephrotic syndrome, hypertension, hematuria, proteinuria, hypoproteinemia, hypercholesterolemia - Late: >2yo a. chronic granulomatous inflammation b. Osteitis of the long bones, maxillofacial and dental malformation c. Keratitis, hearing loss d. Hutchinsons teeth: peg-shaped upper central incisors e. Mulberry molars: excessive # of cusps of molars f. Saddle nose: depression of nasal roof g. Rhagades: spokelike linear scar at mouth, anus, genitalia h. Neuropsychological deficits i. Olympian brow: bony prominence of forehead j. Clavicular/Higoumenakia sign – thick clavicle k. Saber shins: anterior bowing of mid-tibia l. Scaphoid scapula: convex midscapula m. Juvenile paresis: latent CNS infection, focal sz, behavioral changes, MR n. Juvenile tabes: SC, aortitis o. Hutchinson triad: Hutchinson teeth, interstitial keratitis, CN8 deafness p. Clutton joint: painless joint swelling q. Interstitial keratitis: leads to blindness r. CN8 deafness - Blood and lesions: highly infectious until 24h or tx
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How is treponema pallidum diagnosed?
Dx: 1. Darkfield microscopy – for early ds - Definitive dx - Serous transudate from moist lesions a. Primary chancre, condyloma latum, mucus patch, placenta - Consider a suspicious lesion to be nonsyphilitic a. After 3 competent examinations with negative findings - Oral cavity specimen a. Cannot be used b. Nonpathogenic treponemes are part of the oropharyngeal flora 2. Non-treponemal test: screening test a. RPR (rapid plasma reagin) b. VDRL (venereal disease research laboratory) - Detects Ab against Ag on the treponemal surface - Elevated in: active ds, re-infection, tx failure 3. Treponemal tests: confirmatory a. TP-PA: treponema pallidum particle agglutination b. FTA-ABS: fluorescent treponemal Ab absorption c. TP-EIA: pallidum enzyme immunoassay d. MG-TP: microhemagglutination test of Ab to Tpallidum - Useful to confirm dx of 1st episode of syphilis - (+) for life - Measures specific treponeme Ab 4. All pxs should be tested for HIV
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Management
1. Primary, secondary, early latent: - Benzathine pen G 50,000 U/kg IM SD 2. Late latent, tertiary - Ben Pen 50,000-2.4M U IU IM weekly x 3 wks (3 doses) 3. Neurosyphilis - Aqueous crystalline pen G 18-24 M U/d administered as 3-4 M U IV q4h or continuous infusion x 10-14d 4. Congenital Syphillis - Proven: Aqueous Crystalline Penicillin G 100,000- 150,000 U/k/d administered as 50,000 U/k/dose q12 IV on d1-7 then q8h thereafter for a total of 10-15d or Procaine Penicillin G 50,000 U/kg SD x 10-15d - Possible: Aq Penicillin G or Procaine Pen as above for 10d or Benzathin Penicillin G 50,000 U/kg SD IM - Less likely: Ben Pen G 50,000 U/kg IM SD then f/u q2-3 mos for 6 mos
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What is the pathophysiology of HiB?
CH 194: HAEMOPHILUS INFLUENZAE B - Humans are the only natural host - Normal respiratory flora in healthy children - Invasive ds in <5yo - Transmission - Direct contact/ extension from nasopharynx - Inhalation of respi droplet Patho - Polysaccharide capsule major factor in virulence. Encapsulated organism can penetrate the epithelium of the nasopharynx and invade the blood capillaries directly.
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What are the clinical manifestations of HiB?
76 Mgt 1. Primary, secondary, early latent: - Benzathine pen G 50,000 U/kg IM SD 2. Late latent, tertiary - Ben Pen 50,000-2.4M U IU IM weekly x 3 wks (3 doses) 3. Neurosyphilis - Aqueous crystalline pen G 18-24 M U/d administered as 3-4 M U IV q4h or continuous infusion x 10-14d 4. Congenital Syphillis - Proven: Aqueous Crystalline Penicillin G 100,000- 150,000 U/k/d administered as 50,000 U/k/dose q12 IV on d1-7 then q8h thereafter for a total of 10-15d or Procaine Penicillin G 50,000 U/kg SD x 10-15d - Possible: Aq Penicillin G or Procaine Pen as above for 10d or Benzathin Penicillin G 50,000 U/kg SD IM - Less likely: Ben Pen G 50,000 U/kg IM SD then f/u q2-3 mos for 6 mos CH 194: HAEMOPHILUS INFLUENZAE B - Humans are the only natural host - Normal respiratory flora in healthy children - Invasive ds in <5yo - Transmission - Direct contact/ extension from nasopharynx - Inhalation of respi droplet Patho - Polysaccharide capsule major factor in virulence. Encapsulated organism can penetrate the epithelium of the nasopharynx and invade the blood capillaries directly. CM 1. Non-invasive: otitis media (most common cause), sinusitis, conjunctivitis 2. Invasive: bacteremia, meningitis, sepsis 3. Respi: epiglottitis, PNA 4. Cellulitis: preseptal, orbital 5. Suppurative arthritis, osteomyelitis
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What are the diagnostics for HIb?
Dx: 1. GS, C/S 2. Serotyping by agglutination
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How is HIB managed?
Mgt 1. Ampicillin 100-200 mkd IV q6 or ceftriaxone 50-75 mkd IV q12/24 2. Amoxicillin 25-50 mkd po q8/12 – for OM, sinusitis 3. Meningitis: cefotaxime 100-200 mkd IV q6/8, ceftriaxone, ampicillin x 14d for uncomplicated cases 4. High rate of resistance to amipicillin 5. Recommended empiric tx = B-lactam inhibitor combinations, extended spectrum oral cephalosporin
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Give the prophylaxis for HIB
Prophylaxis: - For unvaccinated <48mos child with close contact: - Rifampicin OD 10mkdose x 4d @0-1 mos 20mkdose @ >1mo - Hib conjugate vaccine
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What are streptococcus pneumonia?
Streptococcus pneumonia (pneumococcus) - Gram (+), lancet shaped polysaccharide encapsulated diplococcus - Encapsulated strains cause most serious disease in humans - Important cause of secondary bacterial PN in px with influenza - Major cause of life-threatening PN, meningitis, septicemia
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manifestations of strep pneumonia and management
otitis media, sinusitis, pneumonia and sepsis diagnosis: culture; identification of the organism from the site of infection, blood, or sterile body fluid Management: Meningitis: in px >1month old: Vancomycin IV 60mg/kg/day q6hrs and high-dose Cefotaxime IV 300mg/kg/day q8hrs OR Ceftriaxione IV 100mg/kg/day q12hrs Otitis media: High doses of Amoxiciliin 80-100 mg/kg/day Allergic to Pen: Macrolide or Cotrimoxazole Control measures: use of PCV 13 and PCV 23 vaccines - Tx: penicillin
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MC and only clinically significant GAS org which infects children and adolescents
Group A streptococcus (GAS)/ Streptoccocus pyogenes - MC site of infection = pharynx > skin (pyoderma, impetigo) - Nonsuppurative complications: c. ARF (sequela of pharyngitis, NOT skin infections) d. AGN (sequela of pharyngitis OR skin infections) - CM: acute pharyngitis, impetigo (pyoderma)
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What is Group B streptococcus?
GBS Streptococcus agalactiae: gram (+) aerobic diplococci - 95% of strep infection in infants - Major cause of neonatal bacterial sepsis Group D Streptococcus/Enterococcus - Hospital acquired infection - Gram (+) - N flora of GIT - High abx resistance (ceph, nafcillin, oxacillin, methicillin)
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What are the clinical manifestations of GBS?
CM 1. Sepsis, UTI, peritonitis, meningitis, endocarditis 2. Early-onset: <7d - Milder GBS-like sx, usually full term - 6% mortality 3. Late-onset: >7d - Assoc with extreme PT, IVC, NEC - Severe toxic sx - RD, apnea, bradycardia, deteriorating respiratory function, meningitis - mortality 15% 4. older child: UTI (indwelling catheter)
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Diagnostics?
Dx 1. CBC – leukocytosis, elev neu 2. BCS
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Management of GBS
Mgt: 1. Pen G 100K- 400K ukd IV q4/6 or Ampicillin 100-200mkd IV q6 + Amik 15-22.5 mkd IV q8 2. Vancomycin 40-45 mkd IV q6/8 – if with pen allergy
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How is campylobacter jejuni transmitted and give pathophysiology
CH 202: CAMPYLOBACTER JEJUNI - Ingestion of contaminated poultry, milk, water; pets or farm animals IP: 1-7d Patho - Host conditions assoc with reduced gastric acidity (PPI use), or foods capable of shielding org in transit through the stomach allow Campylobacter to reach intestines à invade and direct damage to mucosal cells through motility (flagellae) à lumen fluid accumulation
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What are the clinical manifestations of campylobacter jejuni?
CM 1. AGE: acute bloody LBM - Fever, headache, myalgia - Watery or bloody mucoid stools - Crampy abdominal pain - Persistent AGE = fecal shedding 2-3w 2. Bacteremia 3. Focal extraintestinal infection - Meningitis, PN, UTI, arthritis, endocarditis, pericarditis 4. Perinatal infection
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Give diagnostics, management and prevention
Dx: 1. Stool CS - >90% sn, DxOC 2. Fecalysis – (+) leukocytes and fecal blood 3. Rectal swab Mgt 1. Erythromycin 40 po q6 x 5d 2. Azithromycin 10mkd po x3d Complic 1. Reactive arthritis 2. GBS
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Give pathophysiology, clinical manifestations and management of Yersinia infection
CH 203: YERSINIA ENTEROCOLITICA - Ingestion of contaminated water/meat, undercooked pigs - Contact of infected animals and blood products - Reservoir: pigs Patho - Ability to form biofilms on surfaces, establish close contact and hijack eukaryotic target cells, and control cellular processes CM: 1. Acute enteritis with mesenteric lymphadenitis - Pseudoappendicitis: Abdominal pain, fever, diarrhea 2. Septicemia Dx: 1. Stool CS, BCS 2. Stool exam – (+) leukocytes Mgt 1. Self-limited: healthy children 2. Ceftriaxone 50-75mkd IV q12/24 + amikacin 15-20mkd IV OD: systemic infection TMP-SMX 8-12 mkd IV/po q12 x 5d is recommended
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most prevalent STD
CH 226: CHLAMYDIA TRACHOMATIS
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Give the clinical manifestations, management and prevention of Chlamydia
Patho - infects columnar epithelial cells à humoral response --> inc IgA, IgG, IgM --> unique biphasic life cycle allows adaptation to both intracellular and extracellular envt CM 1. trachoma: conjunctivitis à scarring à blindness - most important cause of preventable blindness in the world 2. STD - 75% asx’c - Mucoid d/c, PID (20-25%) - May present with urinary sx 3. NB: conjunctivitis, PN Dx: 1. Tissue C/S 2. Fluorescent Ab staining, NAAT, PCR of genital swab or urine Mgt 1. Recommended - Azithromycin 1g po SD - Doxycycline 100mg BID x 7d 2. Alternative - Erythromycin 500mg qid x7d - Levofloxacin 500mg od x7d - Ofloxacin 300mg bid x 7d 3. No sex for 7d after SD azithromycin or until 7d completed regimen and until all partners are treated to minimize reinfection DDx: TB (p. 36) Pertussis (p.46) Pneumonia (p.29) Salmonella (p. 92) Neisseria meningitides (p. 98)
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