Lecture 4: Infectious Disease Flashcards
Osteo Hematogenous spread
2/2 bacteremia (RARE IN ADULTS)
Most common risk factor is IVDU, endocarditis, elderly
Usually long bones or vertebrae are affected
Most commonly mono-microbial (S. aureus in IVDU)
Acute (days to weeks) or chronic course (weeks to months)
Localized bone pain, fever, chills
Osteo direct spread
of bacteria from surrounding tissues (diabetic ulcers, pressure ulcer, puncture wounds, open fractures)
Most common risk factors are DM and PAD
Usually bones of lower extremities are affected
Most commonly poly-microbial including S. aureus, Gram negative and anaerobic
Chronic course
Vague symptoms of localized bone pain or no pain if severe neuropathy
Common places of diabetic ulcers
top of toes, bottoms of toes, pad of foot, heel of foot
Peripheral polyneuropathy (symmetric and distal)
sensory loss – painless ulcers, gait instability. nocturnal pain, burning pain, decreased DTRs, if severe –> motor weakness
Osteomyelitis: Presentation
Acute ( days-weeks), chronic (weeks - months)
Deep bone pain and localized tenderness over the involved area of the bone
Poor wound healing (w/ draining sinuses)
(+/-) erythema and edema
+/- fever, malaise, myalgia, weight loss
Best initial test for osteo?
XRay (periosteal elevation, bone erosions)
If xray is negative but high suspicion
MRI (no CT scan, not very sensitive)
Can’t do MRI then you need this test
bone scan nuclear isotopes which have affinity to osteoblasts (cells that formulate bone) signifies metabolic activity of the bone. Non-specific (maybe positive in metastatic disease, fracture). Obtain if MRI is contraindicated
Why are radiologic tests are not the most accurate tests
don’t know the causative organisms –> Need a bone culture
How do we know If they are improving with osteomylitis?
Follow the ESR, done weekly
first sign of osteomylitis via XRay
Periosteal elevation
MOST EFFECTIVE test for diagnosis of osteomyelitis
MRI will pick up on early infection
ESR , CRP in dx osteomylitis
Non-specific. Usually elevated ( ESR > 70). May suggest the diagnosis. Obtained for monitoring RESPONSE to Rx, DURATION of Rx
Blood culture for dx osteo
only positive 50% of the time
Bone biopsy
MOST ACCURATE TEST to identify microorganisms and guide the therapy
What is the recommended treatment for osteomyelitis?
Delay antibiotics (if possible until culture results are available) Empiric therapy should be broad-spectrum: Vancomycin IV + Ciprofloxacin IV (or Piperacillin/tazobactam IV)
Follow ESR to determine
(1) response to the treatment and (2) duration of the therapy (usually 6-12 weeks) Usually need surgical debridement (+/-) Revascularization
Septic arthritis is an infection of the
synovium, Hematogenous spread (rare in adults) Direct spread of bacteria from surrounding structures (osteomyelitis, skin infection) or contamination of the surgical site (joint replacement)
Risk factors for septic arthritis
degenerative joint (osteoarthritis, rheumatoid arthritis) or artificial joint
Most common pathogen for septic arthritis
S. aureus, disseminated N. gonorrhea (young sexually active adults)
Most commonly affected joint in septic arthritis
knee
Septic arthritis: presentation
Acute onset (hours-days) Rapidly increasing joint pain (ONE JOINT) at rest and with motion (passive rom being limited = joint problem) Joint swollen, warm, tender and red Limited ROM (passive and active), unable to ambulate (+/-) fever
Cellulitis (skin)
Rapid onset and progression over several days. SKIN INFLAMMATION- erythema, edema, warmth, tenderness- hallmark. May or may not be toxic
Osteomyelitis (bone)
Insidious onset, slow progression BONE PAIN (deep)- hallmark POORLY HEALING ULCER/ wound. +/- surrounding erythema, edema, LOCALIZED TENDERNESS Usually non-toxic
Septic arthritis (joint space)
Rapid onset and progression over hours. JOINT –swollen, red, tender, warm. VERY LIMITED ROM, (+) JOINT EFFUSION. May or may not be toxic
WBCs in synovial fluids
1-2k: WNL.
2-20,000: inflammation w/o infection (gout, pseudo-gout)
>50,000: (esp. w/ neutrophils > 80%) infection
Most useful initial test for septic arthritis
Synovial fluids aspiration. WBC is > 50,000 cells with > 80% PMNs (1-2,000 WBC is normal, 2,000-20,000 is inflammatory arthritis like gout). Obtain Gram stain and culture (Ruling out septic)
NAAT for GC
only if gonorrhea is suspected
What is the recommended treatment for septic arthritis?
Start with Vanco IV»_space; f/u cultures» may switch to PO 1st gen. cephalosporin when improvement ( if staph sensitive)
Usually duration - 3- 4 weeks, Joint drainage and “wash out” should be performed
Tx if GC Septic Arthritis
Ceftriaxone 2 gm IV or IM» may switch to PO 3rd gen. cephalosporin when improvement
Lyme disease caused by
spirochete Borrelia Burgdorferi
Lyme transmission
by a tick bite (deer tick Ixodides Scapularis). The tick must be attached for 36-48 hours or more before B. Burgdorferi can be transmitted. 30% patients doesn’t recall tick bite (painless) but recall being outdoors, tick active in the summer in the north east and midwest. Ixodes nymph (young tick) transmits Lyme disease.
Lyme disease within a month
Erythema migrans (90% of patients) , (+/-) flu-like symptoms (fever, headache, myalgia)
Lyme within weeks
Disseminated. Carditis (pericarditis, myocarditis, AV blocks) in <10% of untreated patients Neurologic conditions (meningitis, encephalitis, radiculopathy, cranial nerve palsy) in 10% of untreated patients.
Disseminated infection (months-years) lymes
Migratory arthralgia or arthritis (large joints) in 60% of untreated patients
Erythema migrans
PAINLESS “target” or “bull’s eye” lesion
most common neurologic manifestations of Lyme disease
7th nerve – facial nerve –> motor nerve –> weakness and paralysis. Bell’s palsy – inability to wrinkle brow, drooping eyelid, inability to close eye, inability to puff cheeks, no muscle tone, drooping mouth, cant smile or pucker
What differentiates between Bell’s palsy and a stroke?
Bell’s palsy affects the facial nerve (CN VII) which causes facial weakness in a peripheral pattern (cranial nerves are part of the peripheral nervous system) —that is, weakness involving the lower part of the face( asymmetric smile and flattering of the nasolabial folds) and upper part of the face (flattening of the forehead) . Stroke is caused by ischemia of one the cerebral hemispheres and results in central pattern of the facial paralysis (brain is a part of the central nervous system) that involves only lower part of the face and spares forehead.
Initial test for Lymes?
Target lesions need nothing else. Titers develop later. Igm and IGG for late manifestations
“Gold standard” but rarely positive in Lymes
Cultures (blood, CSF, synovial)
IgM in Lymes
IgM is detected within 6-8 weeks»_space; Negative IgM CAN NOT exclude early disease»_space; Early disease is diagnosed by clinical presentation (rash) and epidemiology (outdoor activity)
IgG in Lymes
IgG develop slowly and persist for life (but do not confer immunity and re-infection may reoccur)»_space; Negative IgG excludes late disease
Diagnosis of Lyme disease
Erythema migrans + outdoor activity in Northeast/Midwest»_space; no tests»_space;proceed for therapy
suspicious for late Lyme disease
Arthritis, neurologic and cardiac symptoms – need IgG titers (positive ELISA should be confirmed by Western blot)
What is the recommended treatment of Lymes with Erythema migrans, Bell’s palsy, Arthritis?
Doxycycline OR Amoxicillin x 14 days
Lymes treatment with Carditis, CNS (meningitis, encephalitis)?
Ceftriaxone 2g/d IV x 14 days
A single dose of Doxycycline 200 mg may be given only if:
endemic region
attached for >36 hours
Antibiotic should be given within 72 hours of tick removal
Removing a tick
Grasp as close to the skin as possible, pull straight up ,do not twist Do not squeeze or crush the tick
Patient education for lymes
Wear long sleeved shirts, long pants (tuck shirts/ pants)
Wear light colors
A nightly “tick check”
Use insect repellant (containing DEET)
Rocky Mountain Spotted Fever ( RMSF)
Rickettsia Rikettsii – gram negative bacteria. Organism enters the host via tick bite (dog tick, wood tick). 30% patients do not report tick bite (painless) RMSF is most likely reported in the southeastern and south central US (“Appalachian fever”) during summer months.
RMSF spreads
R. rickettsii spreads through blood stream > invades endothelial cells»_space; vasculitis (bleeding and microinfarcts) and vascular permeability (edema) Mortality 5-10% (delayed diagnosis)
RMSF caused by a
dog tick (Dermacenter variabilis) transmits R. rickettsii
RMSF clinical manifestations
Acute onset of high fever, severe headache, (+/-) arthralgia. Patients often appear toxic.
Rash begins on the extremities and spreads to the trunk 5 days after symptoms begin (spotted fever): macular that become petechial overtime
Rash with RMSF
Rash starts on extremities and spreads to the trunk (centripetal), initially macular and then petechial
When to suspect RMSF
Fever, headache and rash during SUMMER months + camping/hiking in endemic areas +/- tick bite
Encephlitis s/s
confusion, AMS
Meningitis s/s
sleepy but not Ams, Stiff neck, seizures in late disease
CBC for RMSF
Non-specific. Leukocytosis may be seen
BMP for RMSF
Non-specific. Hyponatremia may be seen in severe cases
Blood cultures for RMSF
R.Rikettsii cannot be cultured
Serology RMSF
Negative serology cannot exclude the disease. IgM- appear 10 days after the onset of illness. It can confirm the dx retrospectively
Immunologic testing of skin biopsy
Determine the presence of R.Rikettsii. Sensitive but not widely available.
CSF analysis
Useful to r/o bacterial meningitis (WBC > 1,000s with predominance of neutrophils) but not to diagnose RMSF meningitis or encephalitis (a lot of other microorganisms may cause WBC is < 1,000 with predominance of lymphocytes)
Dx RMSF
At time of presentation ig M and Igg are negative. Negative test does not rule It out
Take biopsy from lesion send to lab to identify antigen. Diagnosis is clinical
What is the recommended treatment for RMSF?
Start empiric therapy based on clinical grounds (fever, headache during SUMMER months + camping/hiking in endemic areas +/- tick bite) Do not wait until rash appears
Do not wait until antibody appear Doxycycline 200 mg BID (IV» PO) for 7-10 d (INCLUDING children)
Manifestation of Lyme
Flu during SUMMER+ “target” rash ( Erythema migrans) +hiking in endemic areas +/- hx of tick Late manifestation: arthritis, carditis, Bell’s palsy
Manifestation RMSF
Flu during SUMMER + petechial centripetal rash later in the course + hiking in endemic areas+/-hx of a tick bite
Dx Lyme
Early- clinical and epidemiological
Later – serology (negative IgG excludes Lyme)
Dx RMSF
Clinical and epidemiological, may confirm later with serology
Rx Lyme
Doxycycline or Amoxicillin for arthritis and Bell’s palsy IV Ceftriaxone for carditis and meningitis/encephalitis
Rx RMSF
Doxycycline for everyone including children
Cranial Nerves
I – smell (olfactory)
II - see (optic)
III, IV, VI – moves eyes (oculomotor, trochlear, abducens)
V- feels the face (trigeminal)
VII- smile, frown, puff cheeks (facial)
VIII- hear and maintain balance (acoustic)
IX, X- yawn (vagus, glossopharyngeal)
XI- shrug shoulders (accessory)
XII- moves the tongue (hypoglossal)
2 – optic – visual acuity, pupillary reflex and visual fields 5 - facial feels 7 - moves
8 – whisper test 9 & 10 – swallow
