Transcript Bacteria - Cleveland Clinic Regional Hospitals

Bacteria
Dr. Cserynik
Jan. 18, 2007
Slides by Bogdan Irimies
PGY 4 EM Resident
Diptheria: Corynebacterium
diptheriae
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Epidemiology: humans are the only known
reservoirs
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Spread is via person-person contact thru
respiratory droplets or by direct contact
w/skin lesion exudates
0-5 cases nationwide/year
Usually seen unimmunized or under
immunized adults in urban and poor rural
areas
Diphtheria: Corynebacterium
diphtheria
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Etiology/pathophysiology:
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Gram + bacillius: korynee=club shaped
bacteria; diphtheria=leather hide looking
pharyngeal membrane
C. diphtheria produces exotoxin that causes
pharyngeal membrane exudates and systemic
effects of infection
Causes skin, respiratory, cardiac neurological
manifestations
Diphtheria: Corynebacterium
diphtheria
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Incubation period: 1-8 days
Fever, sore throat (thick grayish-black membrane
with sharply defined borders)
Weakness,dysphagia, HA, change in voice,
cervical adenopathy(“bull neck appearance”)
Skin ulcer grayish membrane
Peripheral neuropathy/muscle paralysis
Cardiac: myocarditis, CHF
Diphtheria Membrane:
Diphtheria Bull Neck:
Diphtheria: Corynebacterium
diphtheria
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Complications:
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Airway obstruction from edema/membrane
formation
CHF
Cardiac conduction disturbances
muscle paralysis
Diphtheria: Corynebacterium
diphtheria
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Diagnosis: throat or nasopharyngeal
swabs, cutaneous swabs
PCR for diphtheria gene
Leukocytosis, mild thrombocytopenia,
proteinuria
EKG: ST-T changes, AV block dysrhythmias
Diphtheria: Corynebacterium
diphtheria: D/Dx:
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Strep/viral pharyngitis
Tonsillitis
Vincent’s angina
Epiglottitis
Mono
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Laryngitis
Bronchitis
Tracheitis
Monilial infxn
Rhinitis
Diphtheria: Corynebacterium
diphtheria: Treatment
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Place pt. in respiratory isolation
Bronchodilators, fluids
Equine serum antitoxin is mainstay 20,00040,000 units IV
Erythromycin or procaine penicillin for 14 days
Close contacts should be observed for 7 days,
receive booster of diphtheria toxoid (Td) if >5
yrs.
Pertussis:
Pertussis: Epidemiology
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Localized respiratory illness transmitted by
respiratory droplets
Avg incubation period 7-10 days
Neither vaccination nor prior infection
confer lifelong immunity
Pertussis: Etiology
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Bordetella pertussis, gram neg.
coccobacilli
Preferentially adheres to ciliated
respiratory epithelial cells
Pertussis: Clinical
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Arises in 3 distinct clinical stages:
Catarrhal phase: begins after incubation
period, lasts 1-2 weeks, infectivity is
greatest during this phase
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Clinically indistinguishable from an URI:
rhinorrhea, , low grade fever, malaise,
conjunctival injection, anorexia
Pertussis: Clinical
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Paroxysmal phase: fever subsides and
cough increases(2-4 wks.)
Staccato cough: pt. coughs repeatedly in
short exhalations followed by a short
inspiratory “whoop”
Pt. may have post-tussive emesis,
syncope, brief apnea
Pertussis: Clinical
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Convalescent stage: residual cough that
lasts from several weeks to months
PE: low grade fever and tachypnea
Pertussis: Diagnosis
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Diagnosis should be entertained in anyone
w/prolonged cough w/paroxysmal whoops
or posttussive emesis
Leukocytosis
Lab confirmation by nasopharyngeal swab
or direct fluorescent antibody
Pertussis: D/Dx
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Viral URI
Pneumonia
Bronchiolitis
CF
TB
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COPD Exac.
Foreign Body
Aspiration
Pertussis: Complications
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Periorbital edema
Subconjunctival
hemorrhage
Petechiae
Epistaxis
Hemoptysis
SQ Emphysema
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PTX
Pneumomediastinum
Diaphragmatic
rupture
Hernia exac.
Rectal prolapse
Pertussis:Treatment
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O2, suctioning, hydration
Antibiotics doesn’t appear to reduce the severity
of illness or duration especially if started in
paroxysmal phase
Erythromycin>Azithromax> Bactrim
Postexposure prophylaxis w/erythromycin is
recommended for household contacts of pts.
w/pertussis regardless of previous vaccination
status
Tetanus:
Tetanus: Epidemiology
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Tetanus is a toxin mediated disease
characterized by uncontrolled skeletal muscle
spasms
Avg. 43 cases reported to CDC/year
Most common portals of entry are: puncture
wounds, lacerations, abrasions
Primary risk factors are inadequate primary
immunization and waning immunity
Tetanus: Etiology
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Clostridium tetani gram positive, spore
forming, anaerobic bacillus
Found in soil, dust, feces
Development of clinical tetanus requires a
portal of entry for infecting spores as well
as tissue conditions that promote
germination and growth in an
immunologically susceptible host
Tetanus: Etiology
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C. tetani produces a neurotoxin that causes
clinical illness
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C. tetani produces the neurotoxin tetanospasmin(TS)
at the site of tissue injury
TS binds to the motor nerve ending and then moves
by retrograde axonal transport to the CNS
Preferentially binds to GABA and blocks presynaptic
release of GABA resulting in muscle spasm
Tetanus: Clinical
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Tetanus typically occurs as a result of a
deep penetrating wound
Incubation period is 1 day to several
months
There are 4 types of clinical tetanus:
Generalized, localized, cephalic, and
neonatal
Tetanus: Clinical
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Generalized tetanus:
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Most common form
Trismus(lockjaw), characteristic sardonic
smile(risus sardonicus)
Early symptoms include: irritability, weakness,
myalgias, muscle cramps, dysphagia,
hydrophobia, drooling
Tetanus: Clinical
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Generalized:
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Opisthotonus is a prolonged tonic contraction
that resembles decorticate posturing
Autonomic dysfunction: tachy, HTN, fever,
cardiac dysrythmia and diaphoresis
Opisthotonus:
Sardonic smile:
Tetanus: Clinical
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Localized: persistent muscle spasm
located near site of injury
Most cases do not progress to generalized
tetanus
Tetanus: Clinical
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Cephalic form: rare variant
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Results in cranial nerve palsies and muscle
spasms
Usually ipsilateral to site of injury
Commonly affected nerves: 3, 4,7, 9, 10, 12
Tetanus: Clinical
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Neonatal form: generalized tetanus of
newborn
Symptoms begin during 1st week of life
Irritability and poor feeding seen
Tetanus: Diagnosis
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Clinical diagnosis
No lab test that confirm or exclude disease
CDC clinical case definition:
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“Acute onset of hypertonia or painful muscular
contractions and generalized muscle spasms
without other apparent medical cause.”
Tetanus: D/Dx
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Acute abdomen
Black widow spider bite
Dental
abscess/peritonisillar
abscess
Dislocated mandible/TMJ
Dystonic rxn
meningoencephalitis
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Head trauma/SAH
Hyperventilation
Hypocalcemia
Rabies
Psychogenic
Sepsis
Status Epilepticus
Strychnine poisoning
Tetanus: Complications
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Acute respiratory failure: results from
respiratory muscle spasms, laryngospasm
and airway obstruction
Dysrythmias, HTN, myocarditis, pulm.
Edema
Forceful contractions can cause vertebral
subluxations & fx’s, long bone fx’s,
shoulder & TMJ joint dislocations
Tetanus: Treatment
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4 treatment strategies:
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1.
2.
3.
4.
Aggressive supportive care
elimination of unbound TS
Active immunization
Prevention of further toxin production
Tetanus: Treatment
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Benzodiazepines are DOC for supportive
care
Mechanical ventilation w/neuromuscular
blockade
Autonomic instability: use labetalol
Human tetanus immunoglobulin(TIG)
neutralizes unbound toxin
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Administer at a site separate from toxoid
Tetanus: Treatment
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Administer Td immediately for active
immunization
Prevention of further toxin production is
thru wound debridement and irrigation
Metronidazole is antibiotic of choice
Tetanus: Vaccination
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Tetanus toxoid is an inactivated form of TS
Immunity wanes after 5-10 years
Those younger than 7 years should
receive DPT
No evidence that Td is teratogenic
TIG is not contraindicated in pregnancy
Td Prophylaxis:
Botulism:
Botulism:
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Caused by neurotoxins produced by
Clostridium botulinum
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5 forms of the disease:
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1.
2.
3.
4.
5.
Food born botulism
Infant botulism
Wound botulism
Unclassified botulism
Inadvertent botulism
Botulism: Epidemiology
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7 types of toxins produced but only types
A,B,E,F cause illness in humans
110 cases/year reported to CDC
Food borne botulism results from the
ingestion of preformed heat labile toxin
which is found from exposure to home
canned foods
Botulism: Epidemiology
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Infant botulism is most common form, caused
by ingestion of spores w/in vivo production of
toxin. Found in honey and corn syrup
Wound botulism is rare, 1 case/year, assoc. w/IV
drug abuse
Inadvertent botulism is iatrogenic, occurs in
people who have been injected w/botulism toxin
for dystonia, movement disorders and cosmetic
purposes
Botulism: Etiology
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C. botulinum anaerobic, gram positive rod
Bacteria produces a potent exotoxin that is
responsible for the disease
Botulinum toxin targets peripheral
neuromuscular junctions and autonomic
synapses causing flaccid paralysis
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Blocks the release of acetylcholine resulting in
neuromuscular blockade
Botulism: Clinical
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Botulism manifests by cranial nerve
palsies, parasympathetic blockade,
descending flaccid paralysis
Food borne botulism is prototype of
disease
Symptoms begin 18-36 hrs. after ingestion
of toxin containing food
Botulism: Clinical
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Early symptoms include weakness,
malaise, lightheadedness, N/V,
constipation
Neurologic symptoms: cranial nerves
affected
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Diplopia, blurry vision, dysphonia, dysphagia,
dysarthria
Symmetric descending muscular weakness
occurs involving upper and lower extremities
and respiratory muscles
Botulism: Clinical
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Ocular signs: ptosis, extraocular palsies,
dilated & fixed pupils
Muscle weakness: upper extremities more
affected than lower, proximal
weakness>distal muscles
Sensory exam is normal
Botulism: Clinical
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Infant botulism:
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Constipation is common symptom, poor
feeding, weak cry, loss of head control,
hypotonia, decreased muscle tone, depressed
deep tendon reflexes
Wound botulism: incubation period is
longer 4-14 days
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Clinical presentation is similar to food borne
botulism
Infant Botulism:
Wound Botulism:
Botulism: Diagnosis
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Initial diagnosis is clinical: suspect in
someone who presents with constellation
of GI, Autonomic, cranial nerve
dysfunction
Confirmed by:
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1. botulinum toxin in pts. Blood
2. Botulinum toxin or C. botulinum in GI
contents, stool, or wound
3. Toxin in the food source
Notify CDC
Botulism: D/Dx
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Pharyngitis
Gastroenteritis
Guillain Barre Syndrome
Tick paralysis
Myasthenia Gravis
Poliomyelitis
Diphtheria
Eaton Lambert Syndrome
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Anticholinergic toxicity
Organophosphate toxicity
Heavy metal poisoning
Mg+2 toxicity
Botulism: Complications
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Complications are related to respiratory
failure
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Weakness of respiratory muscles
Botulism: Treatment
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Treatment consists of: supportive care,
administer antitoxin
ICU, NG tube, foley
Antitoxin: contains antibodies to toxins
types A,B, E
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Neutralizes only circulating toxins and has no
effect on bound toxin
One vial is required
Botulism: Treatment
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Infant botulism: antitoxin is not
recommended b/c not efficacy, there is a
risk of anaphylaxis to horse serum
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Use human botulism immunoglobulin(BIG)
Wound botulism:
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Debridement and antibiotics should be given
only after antitoxin has been given
Pneumococcus:
Pneumococcemia:
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Strep. Pneumoniae: clinical presentation
ranges from mild illness to fulminant, life
threatening systemic syndrome
Also causes localized infections such as:
OM, pneumonia, meningitis, endocarditis,
septic arthritis, peritonitis.
Strep. Pneumoniae:
Epidemiology
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Exact incidence is unknown. Spread from
person to person by close contact
The introduction of the heptavalent
vaccine has decreased incidence of
disease by 69% in children < 2 y/o
Risk Factors for pneumococcemia: chronic
respiratory or CV disease, chronic ETOH
abuse, cirrhosis, DM, impaired
spleen(sickle cell), CRF, AIDS, cancer,
organ transplant
Strep. Pneumoniae: Etiology
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Encapsulated, gram positive anaerobic
coccus that occurs in pairs and chains
Over 90 serotypes
Prevnar vaccine account for 7 serotypes
which cause 80% of invasive disease in
children
Pneumococcus:
Strep. Pneumoniae: Etiology
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Strep Pneumo enters bloodstream by one
of two routes:
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1. Begins as pulmonary infection, thru
lymphatics and into bloodstream
2. Colonizes or cause URI and spreads to
Subarachnoid space, then to arachnoid villi to
venous sinus to blood
Can cause a clinical picture from a minor
febrile illness to septic shock
Strep. Pneumoniae: Clinical
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Presents as SIRS syndrome
Also may present as lethargy, signs of
poor tissue perfusion, cyanosis,
hypo/hyperventilation
Findings on physical exam vary with site
of localized infection
Strep. Pneumoniae: Diagnosis
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The only specific test is blood culture
Check CBC w/diff, blood & urine cultures,
electrolytes, CXR, sputum, ABG prn, LP
prn, coags prn
Strep. Pneumoniae: Complications
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CV collapse, DIC, Septic emboli,
Respiratory failure, meningitis,
hypothermia, GI Bleeding, hepatic coma,
renal failure, MI
Pneumococcemia can cause
hematogenous seeding which results in:
peritonitis, arthritis, endocarditis,
meningitis, cellulitis
Strep. Pneumoniae: Treatment
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Prompt initiation of antibiotics: Penicillin G,
ceftriaxone(covers also N. meningitis, H.
flu)
PCN allergic pt: cefotaxime, ceftriaxone,
vanco, chloramphenicol
For PCN resistant Strep. Pneumo: use
ceftriaxone, cefotaxime, vancomycin or
imipenem
For suspected pneumococcal meningitis:
use vanco + cefuroxime or cefotaxime
Pneumococcal Vaccine:
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Effective in preventing disease, accounts
for 85-90% of pneumococcus infections
Recommended for children ages 2-23
months
Recommended for adults with the
following:
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Chronic illness: CV/Pulm, DM, ETOHics
Immunocompromised people including
asplenic pts.,HIV
Meningococcemia:
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Think of this in a patient who appears
relatively well on initial presentation, then
becomes morbiund and critically ill
w/fulminant infection several hours later
Meningococcemia: Epidemiology
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2400-3000 cases annually
Crowded living conditions increase the
risk: military recruits, college freshman
Risk Factors: close contact w/an infected
pt., complement def., asplenia, chronic
ETOH abuse, smoking, chronic steroid
use, recent respiratory infection
Overall mortality rate is 10%!
Meningococcemia: Etiology
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Caused by Neisseria meningitidis a gram neg.
diplococcus, aerobic, encapsulated organism
w/13 serotypes
N. meningitidis attaches to nonciliated epithelial
cells in the nasopharynx and either becomes an
asymptomatic carrier state or produces a mild
URI syndrome.
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If it enters the bloodstream: may see localized
infection, bacteremia, sepsis or fulminant infection
Meningococcemia: Clinical
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Clinical presentation ranges from mild
febrile illness to fulminant disease and
death w/in hours
May see fever, irritability, lethargy,
myalgias, emesis, diarrhea, cough,
rhinorrhea
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Only 60% of pts. Have classic signs of
meningococcemia: fever, petechiae or purpura
Meningococcemia: Clinical
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Meningococcal meningitis may present as fever,
HA, photophobia, vomiting and signs of
meningeal inflammation
Infants and small children may present as fever,
irritability, vomiting
Purpura fulminans: occurs in children, usually
assoc. w/DIC.
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characterized by rapidly spreading ecchymosis and
gangrene of the extremities
Purpura:
Petechiae:
Meningococcemia: Clinical
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Fulminant meningococcemia: Waterhouse
Friderichsen Syndrome
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Extreme severity of illness, shock like state
Diffuse petechiae and purpuric rash
Shock, CHF, DIC, Renal failure, coma possible
Bilateral adrenal hemorrhage
Meningococcemia: Diagnosis
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Diagnosis of N. meningitidis is confirmed
by isolation from blood cultures, CSF,
synovial, pleural or pericardial fluid
WBC count may be high, low or normal
Bandemia is typically present
Meningococcemia: D/Dx
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Strep. Pneumo
H. Flu
N. Gonorrhea
Viral exanthem
RMSF
Typhus
Endocarditis
Vasculitis(HSP)
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Toxic Shock
Acute Rheumatic
fever
Drug rxns
ITP
TTP
Meningococcemia:
Complications
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Most common complication is myocarditis
w/CHF or conduction abnormalities
Respiratory failure
Renal failure
Cranial nerve palsies
Vasculitis
Purulent arthritis
Meningococcemia: Treatment
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Immediate antibiotics: lab ID use PCN G
or ampicillin
Alternatives are: cefotaxime, ceftriaxone,
chloramphenicol
Airway mgmt, IVF support and
vasopressor support, glucocorticoid
therapy for refractory shock
Meningococcemia: Prophylaxis &
Vaccination
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Antibiotic prophylaxis for close contacts
such as household, nursery school,
daycare, intimate contacts, health care
workers
Use rifampin for 4 doses or Cipro
Vaccine to children 2 years or older in high
risk groups such as functional or anatomic
asplenia or complement def.
Kawasaki’s Disease:
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KD is an acute febrile systemic vasculitis
of unknown etiology
Also called Acute Febrile Mucocutaneous
Lymph Node Syndrome
Kawasaki’s Disease:
Epidemiology
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Peak incidence is in 1-2 year olds
Most prevalent in Asian descent
3000 cases annually
Overall mortality is 2.5% and is a result of
cardiac complications
Kawasaki’s Disease: Etiology
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KD is a systemic vasculitis
There is some link between mechanism of
vascular injury and immune system
activation
Vasculitis affects medium sized vessels
Inflammation in the coronary arteries can
cause myocarditis and aneurysms
Kawasaki’s Disease: Clinical
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Fever for at least 5 days and four of the following 5
signs:
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1. Bilateral conjunctival injection
2. Oral mucosa changes
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3. Hand and feet changes
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Erythematous dry fissured lips
Strawberry tongue
Erythematous oropharynx
Erythema of palms & soles
Edema of hand & feet
Periungal desquamation
4. Rash
5. Cervical lymphadenopathy
Mucocutaneous involvement:
Edema of hands:
Kawasaki’s Disease: Clinical
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Cardiac involvement is the hallmark of the
disease:
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KD is most common cause of acquired
pediatric heart disease in U.S.
May see myocarditis, CHF, Tachycardia
Coronary artery aneurysms
Mortality is from coronary artery aneurysm
rupture or MI
Coronary Artery Aneurysm:
Kawasaki’s Disease: Diagnosis
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Fever > 5 days plus 4/5 criteria
No definitive test
EKG, Echo
CBC, CRP, ESR, CMP w/LFT’s
May see elevated WBC w/left shift,
normochromic normocytic anemia, elevated plt
ct> 1,000,000
Pts. w/KD should have UA, blood cx, CXR, ASO
titer, GABHS throat cx to exclude other diagnosis
Kawasaki’s Disease: D/Dx
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Measles
Toxic shock
Scarlet Fever
Leptospirosis
Stevens Johnson
Syndrome
Staph. Scalded skin
syndrome
Influenza
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RMSF
Juv. RA
Drug rxn
Viral infection
Mercury toxicity
Retropharyngeal
abscess
GABHS infections
Kawaski’s Disease:
Complications
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Coronary artery aneurysm is most serious
complication
Occurs in 20-25% of untreated pts.,
occurs in 3-4% of those treated w/IV
immunoglobulin and ASA
Other complications: MI, CHF, myocarditis
Kawasaki’s Treatment:
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Hospitalize pt.
Includes administration of ASA and IV
gamma globulin
ASA 80-100mg/kg/day for 6-8 wks
If coronary artery abnormalities exist, can
use dipyridamole

Coumadin or heparin for severe coronary
disease
Toxic Shock Syndrome:
Epidemiology
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Toxic Shock Syndrome is a toxin mediated
systemic inflammatory response syndrome
Menstruation remains most common
setting
200 cases a year
Nonmenstrual TSS is assoc.
w/superinfection of various skin
lesions/soft tissue infections: strep TSS
Mortality rate of staph TSS is 3%, strep
TSS is 30-70%
Toxic Shock Syndrome: Etiology
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Staphylococcal TSS is caused by colonization or
infection w/toxigenic strains of S. aureus
Streptococcal TSS is caused by infection
w/toxigenic strains of group A strep(GAS).
Staph. Aureus produces toxic shock syndrome
toxin(TSST-1)
GAS produces streptococcal pyrogenic exotoxin
Toxic Shock Syndrome: Risk Factors
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Use of super
absorbent tampon
Post-op wound
infection
Post-partum period
Nasal packing
Bacterial infections
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Varicella or Influenza
A infection
DM
HIV
Chronic cardiac &
pulmonary disease
Toxic Shock Syndrome: Case
Definition for Staph. Aureus TSS
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Fever >38.9C
Diffuse erythroderma rash
Palm and sole desquamation rash 1-2 wks later
Hypotension
Multisystem involvement: 3 or more of following
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GI: N/V/D
Muscular: myalgias or incr. CPK
Mucus Membrane hyperemia
Renal: elevated BUN/Cr.
Hepatic: elevated LFT’s, bili
Heme: plts. <100,000
CNS: Altered mental status
Toxic Shock Syndrome: Case
Definition for Strep TSS
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Isolation of group A strep from body site
Clinical signs: 2 or more
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Hypotension and
Renal impairment
Coagulopathy
Liver abnormalities
ARDS
Necrotizing fasciitis
Erythematous rash
TSS: Clinical
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The clinical presentations of strep TSS and
staph TSS are similar
The primary difference is an identifiable
infectious source is always present w/strep
TSS and colonization alone may be the
only source in staph TSS
TSS: Clinical
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Fever, chills
N/V/D
Myalgias
Pharyngitis
HA
Sepsis w/organ
dysfunction
Rash
Altered mental status
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Conjunctival erythema
Strawberry tongue
Peripheral edema
Erythematous rash:
TSS: Diagnosis
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See case definitions
May see leukocytosis or leukopenia,
bandemia
CXR
LP prn
EKG
TSS: D/Dx
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Kawasaki’s Disease
Staph Scaled skin
syndrome
Scarlet fever
Drug rxns/Stevens
Johnson
RMSF
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Leptospirosis
Meningococcemia
Gram neg. sepsis
Measles
Viral illness
TSS: Complications
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ARDS
Shock
Gangrene
DIC
Rhabdo/Renal failure
Seizures
Pancreatitis
Pericarditis
Cardiomyopathy
Neuropsychiatric symptoms
TSS: Management
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Aggressive fluids
O2, monitor
Source of bacteria removed(tampons,
nasal packing, wound debridement)
Antibiotics: clinda, nafcillin or oxacillin
Refractory case use IV immunoglobulin
Summary:
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All pts. Appearing septic should be treated w/broad
spectrum antibiotics ASAP
Immunity to Diphtheria, pertussis, tetanus wanes in
adults. Think of pertusssis as a cause of persistent cough
in adults. Update Td in trauma or infection
Botulism should be in differential for infant who presents
w/failure to thrive, constipation or decreased muscle
tone. Also in IV drug abuser w/neurologic symptoms
IV GG should be given as soon as KD is diagnosed