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Internal Medicine > Step Up - Infectious Diseases > Flashcards

Step Up - Infectious Diseases Flashcards

1
Q

Nosocomial pneumonia - Definition:

A

Occurs after the first 72h of hospitalization.

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2
Q

Classic CAP presents with:

A
  1. Sudden chill.
  2. Fever.
  3. Pleuritic pain.
  4. Productive cough.
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3
Q

Atypical pneumonia - Presents with:

A

Often begins with a sore throat and headache followed by a non productive cough and dyspnea.

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4
Q

2 recommended methods of prevention:

A
  1. Influenza vaccine - Give yearly to people at incr. risk for complications and to health care workers.
  2. Pneumococcal vaccine - For patients >65yr and for younger people at high risk (eg those with heart disease, sickle cell disease, pulmonary disease, diabetes, alcoholic cirrhosis, asplenic individuals).
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5
Q

Typical CAP - Common agents:

A
  1. S.pneumoniae (60%).
  2. H.influenza (15%).
  3. Aerobic gram(-) rods (6-10%) - Klebsiella (and other Enterobacteriaceae).
  4. S.aureus (2-10%).
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6
Q

Typical CAP - Clinical features - Symptoms:

A
  1. Acute onset of fever and shaking chills.
  2. Cough productive of thick, purulent sputum.
  3. Pleuritic chest pain (suggest pleural effusion).
  4. Dyspnea.
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7
Q

Typical CAP - Signs:

A
  1. Tachycardia, tachypnea.
  2. Late inspiratory crackles.
  3. Bronchial breath sounds
  4. Incr. tactile vocal fremitus.
  5. Dullness on percussion.
  6. Pleural friction rub (associated with a pleural effusion).
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8
Q

Most cases of CAP result from?

A

Aspiration of oropharyngeal secretions because the majority of organisms that cause CAP are NORMAL INHABITANTS of the pharynx.

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9
Q

CXR - Typical CAP:

A
  1. Lobar consolidation.

2. Multilobar consolidation indicates very serious illness.

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10
Q

General approach to diagnosis of CAP - 1st step:

A

Differentiate lower respiratory tract infection from the other causes of cough and from upper respiratory tract infection.

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11
Q

General approach to diagnosis of CAP - 2nd step - Once lower tract infection is suspected:

A

Next task is to differentiate between pneumonia and acute bronchitis - Clinical features NOT reliable - CXR the only reasonable method of differentiating between pneumonia and acute bronchitis.

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12
Q

Studies have shown that if VITAL SIGNS are entirely normal, the probability of pneumonia in outpatients is less than?

A

1%.

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13
Q

Atypical CAP - Common agents:

A
  1. Mycoplasma pneumoniae (MC).
  2. Chlamydia pneumoniae.
  3. Chlamydia psittaci.
  4. Coxiella burnetti (Q fever).
  5. Legionella spp.
  6. Viruses - Influenza (A, B), adenoviruses, parainfuenza virus, RSV.
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14
Q

Atypical CAP - Clinical features - Symptoms:

A
  1. Insidious onset - headache, sore throat, fatigue, myalgia.
  2. Dry cough (no sputum production).
  3. Fevers (chills are uncommon).
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15
Q

Atypical CAP - Clinical features - Signs:

A
  1. Pulse-Temperature dissociation - normal pulse in the setting of high fever is suggestive of atypical CAP.
  2. Wheezing, rhonchi, crackles.
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16
Q

Atypical CAP - CXR:

A
  1. Diffuse reticulonodular infiltrates.

2. Absent or minimal consolidation.

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17
Q

Sputum culture CAP:

A

The value of routine sputum collection for Gram stain and culture is controversial. The Infectious Disease Society of America has recently advocated performing sputum Gram stain and culture in ALL patients hospitalized with CAP.

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18
Q

The following steps are appropriate in patients admitted to the hospital with suspected pneumonia:

A
  1. CXR (PA and lateral).
  2. Lab tests - CBC and differential, BUN, Cr, glucose, electrolytes.
  3. SaO2.
  4. Two pretreatment blood cultures.
  5. Gram stain and culture of sputum.
  6. Antibiotic therapy.
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19
Q

Diagnosis of pneumonia - CXR:

A
  1. PA and lateral CXR REQUIRED to confirm the diagnosis.
  2. Considered sensitive - If CXR findings are NOT suggestive of pneumonia, do not treat the patients with antibiotics.
  3. After treatment, changes evident on CXR usually lag behind the clinical response (up to 6wks).
  4. Changes include interstitial infiltrates, lobar consolidation, and/or cavitation.
  5. False-negative chest radiographs occur with neutropenia, dehydration, infection with PCP, and early disease <24h.
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20
Q

Do radiographic changes and clinical findings help in identifying the causative organism in CAP?

A

No, they do not help.

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21
Q

Pneumoniae pearls:

A
  1. Alcoholics –> Klebsiella.
  2. Immigrants –> TB.
  3. Nursing home residents –> Nosocomial pathogen and predilection for the upper lobes (eg Pseudomonas).
  4. HIV(+) –> PCP + TB - still more likely to have a TYPICAL infectious agent.
  5. Legionella –> Organ transplant recipients, renal failure, chronic lung disease, smokers.
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22
Q

Diagnosis of pneumonia - Sputum Gram stain:

A

Try to obtain in all patients:

  1. Commonly contaminated with oral secretions.
  2. A good specimen has a sensitivity of 60% and specificity of 85% for identifying gram(+) cocci in chains (S.pneumoniae).
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23
Q

Diagnosis of pneumonia - Sputum culture:

A

Try to obtain in all patients REQUIRING hospitalization - Specificity is improved if the predominant organism growing on the culture media correlates with the Gram stain.

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24
Q

Diagnosis of pneumonia - Special stains of the sputum in selected cases:

A
  1. Acid-fast stain (Mycobacterium spp.) if TB is suspected.

2. Silver stain (fungi, Pneumocystis carinii) for HIV/immunocompromised.

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25
Q

Diagnosis of pneumonia - Urinary antigen assay for Legionella in selected patients:

A
  1. Test is VERY SENSITIVE.

2. Antigen persists in the urine for WEEKS (even after treatment has been started).

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26
Q

Diagnosis of pneumonia - Blood cultures:

A

Positive in 5%-15% of cases.

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27
Q

Test for microbial diagnosis for outpatients?

A

NOT required - Empiric treatment is often successful if CAP is suspected.

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28
Q

Treatment of CAP - Decision to hospitalize:

A

The decision to hospitalize or treat as an outpatient is probably the MOST IMPORTANT decision to be made and is based on severity of disease.

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29
Q

Uncomplicated CAP in patients WITHOUT significant comorbidities - Treat with:

A

Azithromycin or Clarithromycin (if comorbidities, give a fluoroquinolone).

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30
Q

Treatment of pneumonia - In people younger than 60yrs:

A

MC organisms are: S.pneumoniae, Mycoplasma, Legionella, Chlamydia.

  • -> Macrolides (azithromycin, clarithromycin) or doxycyclin cover ALL of these organisms and are the first-line treatment.
  • -> Alternative: Fluoroquinolones.
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31
Q

Treatment of pneumonia - In older adults and patients with comorbidities (more likely to have typical CAP) OR those treated with antibiotics in the last 3 months, treat with:

A

First-line agent –> Fluoroquinolone (levofloxacin, moxifloxacin).

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32
Q

Treatment of pneumonia - For outpatient, treatment is continued for?

A

5 days. DO NOT stop treatment until patient has been afebrile for 48h.

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33
Q

Treatment of pneumonia - Hospitalized patients:

A

A fluoroquinolone alone or a 3rd-gen cephalosporin + macrolide (ceftriaxone + azithromycin) is appropriate.

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34
Q

Treatment of hospital-acquired pneumonia:

A

Treatment is tailored toward gram(-) rods (any of the following are appropriate):

  1. Cephalosporins with pseudomonal coverage: ceftazidime, cefepime.
  2. Carbapenems: imipenem.
  3. Piperacillin/tazobactam
    - -> Macrolides are NOT used - as they are in CAP.
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35
Q

Complications of pneumonia:

A
  1. Pleural effusion (“parapneumonic effusions”).
  2. Pleural empyema occurs in 1%-2% of all cases of CAP (up to 7% of hospitalized patients with CAP).
  3. Acute respiratory failure may occur if the pneumonia is severe.
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36
Q

Complications of pneumonia - Pleural effusion:

A
  1. Can be seen in >50% of patients with CAP on routine CXR. Empyema is infrequent in these patients.
  2. Most of these effusions have an uncomplicated course and resolve with treatment of the pneumonia with antibiotics.
  3. Thoracentesis should be performed if the effusion is significant (>1cm on lateral decubitus film) –> Send fluid for Gram stain, culture, pH, cell count, determination of glucose, protein, and LDH.
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37
Q

Ventilator associated pneumonias - Risk:

A
  1. Normal mucociliary clearance of the respiratory tract is impaired (cannot cough).
  2. Also, positive pressure impairs the ability to clear colonization.
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38
Q

Ventilator associated pneumonia - Findings:

A
  1. New infiltrate on chest X-ray, purulent secretions from endotracheal tube.
  2. Fever.
  3. Rising WBC count.
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39
Q

Ventilator associated pneumonia - Treatment:

A

Combination of the following 3 different drugs:

  1. Cephalosporin (ceftazidime or cefepime) OR penicillin (piperacillin/tazobactam) OR carbapenem (imipenem).
  2. Aminoglycoside OR fluoroquinolone.
  3. Vancomycin OR linezolid.
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40
Q

Lung abscess Pearls:

A
  1. Areas most likely to be infected by aspirated material - POSTERIOR segments of the UPPER lobes and SUPERIOR segments of the LOWER lobes.
  2. Aspirated material is more likely to affect the RIGHT lobe due to angle of the right main stem bronchus from the trachea.
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41
Q

Lung abscess - Typical case:

A

The typical case is aspiration of a large volume of oropharyngeal contents or food, with resulting pneumonia and necrosis when adequate treatment is NOT administered.

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42
Q

By definition, a lung abscess is formed by?

A

One or more cavities, each >2cm in diameter.

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43
Q

Lung abscesses can be complications of the following:

A
  1. Aspiration of organisms.
  2. Acute necrotizing pneumonia.
  3. Hematogenous spread of infection from distant site.
  4. Direct inoculation with contiguous spread.
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44
Q

Lung abscess - Causative organisms:

A

Bacteria that colonize the oropharynx:

  1. Oral anaerobes: Prevotella, Peptostreptococcus, Fusobacterium, Bacteroids spp.
  2. Other: S.aureus, S.pneumoniae, and aerobic gram(-) bacilli.
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45
Q

Lung abscesses - Epidemiology/risk factors:

A
  1. Main risk factor is predisposition to aspiration.
  2. Poor dental hygiene.
  3. Edentulous patients are less likely to aspirate oropharyngeal secretions.
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46
Q

Lung abscesses - Clinical features:

A
  1. Majority –> Indolent course. Some present more acutely.
  2. Cough - Foul-smelling sputum is consistent with ANAEROBIC infection - Sometimes blood-tinged.
  3. Fever, chills.
  4. Constitutional symptoms: Fatigue, malaise, weight loss.
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47
Q

Lung abscess - Diagnosis - CXR:

A

Reveals thick-walled cavitation with air-fluid levels.

–> Look for abscess in dependent, poorly ventilated lobes.

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48
Q

Lung abscess - Diagnosis - CT:

A

May be necessary to differentiate between abscess and empyema.

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49
Q

Lung abscess - Diagnosis - Culture:

A

Consider obtaining cultures via bronchoscopy or transtracheal aspiration rather than simple expectoration to avoid contamination with oral flora.

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50
Q

Lung abscess - Treatment:

A
  1. Hospitalization is often required if lung abscess is found. Postural drainage should be performed.
  2. Antimicrobial therapy.
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51
Q

Lung abscess - Antimicrobial therapy:

A
  1. Antibiotic regimens include coverage for the following:
    a. Gram(+) cocci - ampicillin or amoxicillin/clavulanic acid, ampicillin/sulbactam, or vancomycin for S.aureus.
    b. Anaerobes - Clindamycin or metronidazole.
    c. If Gram(-) are suspected - Add fluoroquinolone or ceftazidime.
  2. CONTINUE antibiotics until the cavity is gone or until CXR findings have improved considerably.
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52
Q

Lung abscess - Antimicrobial therapy - How long may it take?

A

This may take months!

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53
Q

TB - Transmission:

A
  1. Occurs via inhalation of aerosolized droplets containing active organism.
  2. Only those with active TB are contagious (eg by coughing, sneezing).
  3. People with primary TB are NOT contagious.
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54
Q

Percentage of people with primary TB that will develop active disease in their lifetime?

A

Only 5-10%.

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55
Q

TB - Risk factors:

A
  1. HIV(+)
  2. Recent immigrants (within past 5yrs).
  3. Prisoners
  4. Health care workers
  5. Close contacts of someone with TB.
  6. Alcoholics
  7. Diabetics
  8. Glucocorticoid use
  9. Hematologic malignancy
  10. Injection drug users.
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56
Q

Primary TB - Clinical features:

A
  1. Asymptomatic.
  2. Pleural effusion may develop.
  3. If the immune response is incomplete, the pulmonary and constitutional symptoms of TB may develop. This is known as progressive primary TB.
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57
Q

Primary TB - Radiographic findings:

A
  1. Ghon’s complex - calcified primary focus with an associated lymph node.
  2. Ranke’s complex - when Ghon’s complex undergoes fibrosis and calcification.
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58
Q

Extrapulmonary TB - Sites:

A
  1. Lymph nodes.
  2. Pleura.
  3. GUT.
  4. Spine
  5. Intestine.
  6. Meninges.
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59
Q

Diagnosis of TB is challenging in HIV patients because:

A
  1. PPD skin test result is negative.
  2. Patients have “atypical” CXR findings.
  3. Sputum smears are more likely to be negative.
  4. Granuloma formation may NOT be present in the late stages.
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60
Q

Diagnosis of TB - CXR:

A
  1. Classic –> Upper lobe infiltrates with cavitations.
  2. Other possible findings:
    a. Pleural effusion.
    b. Ghon’s complex and Ranke’s complex - evidence of healed primary TB.
    c. Atypical findings common in immunocompromised patients.
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61
Q

Diagnosis of TB - Sputum studies:

A
  1. DEFINITIVE diagnosis is made by sputum culture - growth of M.tuberculosis.
  2. Obtain 3 morning sputum specimens - culture takes 4-8wks.
  3. PCR can detect more rapidly.
  4. Diagnosis sometimes made by finding AFB on microscopic exam, but this is NOT definitive because other mycobacteria may colonize airways.
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62
Q

If PPD test is positive, what should be done?

A

A CXR to rule out active disease. Once active disease is EXCLUDED, 9 months of INH treatment is initiated (!).

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63
Q

A patient with a positive PPD test has how much lifetime risk of TB?

A

A 10% lifetime risk of TB –> This risk is reduced to 1% after 9months of INH treatment.

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64
Q

If patient has been BCG vaccinated, and we find positive PPD, do we give INH?

A

Yes, for 9 months, REGARDLESS of the BCG vaccination.

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65
Q

TB Treatment - Patients with active TB must be ISOLATED until sputum is negative for AFB. First-line therapy:

A 
4-drug regimen:
1. INH
2. Rifampin
3. Pyrazinamide
4. Ethambutol or streptomycin
FOR 2 MONTHS!
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66
Q

TB Treatment - After the initial 2 month phase?

A

A phase of 4 MONTHS is recommended using INH and rifampin.

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67
Q

Prophylactic treatment for latent (primary) TB:

A

Consists of 9 months of INH after active TB has been excluded (negative CXR, sputum, or both).

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68
Q

ALL TB medications can cause?

A

Hepatotoxicity. Discontinue treatment only if liver transaminases rise to 3-5times the upper limit or normal.

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69
Q

Influenza - Transmission:

A

Orthomyxovirus –> Transmitted via respiratory droplets, typically occurring in winter months.

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70
Q

Influenza - Clinical findings:

A

Rapid onset of:

  1. Fever
  2. Chills
  3. Malaise
  4. Headache
  5. Non productive cough
  6. Sore throat
  7. Nausea may also be present
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71
Q

Meningitis - Pathophysiology:

A
  1. Infectious agents –> Frequently colonize the nasopharynx and respiratory tract.
  2. These pathogens enter the CNS.
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72
Q

Meningitis - How do pathogens enter the CNS?

A
  1. Invasion of the bloodstream, which leads to hematogenous seeding of the CNS.
  2. Retrograde transport along cranial (eg olfatory) or peripheral nerves.
  3. Contiguous spread from sinusitis, otitis media, surgery, or trauma.
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73
Q

Acute meningitis:

A

Onset within hrs to days.

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74
Q

Chronic meningitis:

A

Onset within weeks to months - commonly caused by mycobacteria, fungi, Lyme, or parasites.

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75
Q

Acute bacterial meningitis - Complications:

A
  1. Seizures
  2. Coma
  3. Brain abscess
  4. Subdural empyema
  5. DIC
  6. Respiratory arrest
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76
Q

Acute bacterial meningitis - Complications - Permanent sequelae:

A
  1. Deafness
  2. Brain damage
  3. Hydrocephalus
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77
Q

Aseptic meningitis - Etiology:

A
  1. Enteroviruses
  2. HSV
  3. Also by certain bacteria, parasites, fungi
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78
Q

Acute bacterial meningitis is a…?

A

MEDICAL EMERGENCY! Frequently fatal, even with appropriate treatment.

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79
Q

Acute bacterial meningitis - clinical features:

A

Characteristic triad:

  1. Fever
  2. Nuchal rigidity
  3. Change in mental status
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80
Q

Meningitis - Symptoms:

A
  1. Headache (may be more severe when lying down).
  2. Fevers.
  3. Nausea and vomiting.
  4. Stiff, painful neck.
  5. Malaise.
  6. Photophobia.
  7. Alteration in mental status (confusion, lethargy, even coma).
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81
Q

Meningitis - Signs:

A
  1. Nuchal rigidity (may be ABSENT).
  2. Rashes - Maculopapular with petechiae –> PURPURA is classic for N.meningitidis/ Vesicular lesions in varicella or HSV.
  3. Incr. ICP and its manifestations - papilledema, seizures.
  4. Cranial nerve palsies.
  5. Kernig (only in 50%) and Brudzinki (only in 50%).
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82
Q

Diagnosis of meningitis - LP or CT first?

A

CT of the head, first –> If there are focal neurologic signs or if there is evidence of a space-occupying lesion with elevations in ICP.

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83
Q

Meningitis - Prophylaxis:

A
  1. Rifampin
  2. Ceftriaxone
    for all close contacts of patients with meningococcus, give 1 dose of IM ceftriaxone.
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84
Q

Meningitis Treatment - Infants:

A

Cefotaxime + ampicillin + vanco (aminoglycoside if <4weeks).

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85
Q

Meningitis Treatment - 3mo to 50yrs:

A

Ceftriaxone or cefotaxime + Vancomycin.

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86
Q

Meningitis Treatment - >50yrs:

A

Ceftriaxone or cefotaxime + vancomycin + ampicillin.

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87
Q

Meningitis Treatment - Impaired cellular immunity (eg HIV):

A

Ceftazidime + Ampicillin + Vancomycin.

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88
Q

Encephalitis is often seen together with…?

A

Meningitis

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89
Q

Encephalitis - Viral causes:

A
  1. HSV-1
  2. Arbovirus - Eastern equine encephalitis, West Nile virus.
  3. Enterovirus - polio.
  4. Less common causes - Measles, mumps, EBV, CMV, VZV, rabies, prion diseases such as Creutzfeldt-Jakob.
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90
Q

Encephalitis - NON viral infectious causes:

A
  1. Toxoplasmosis.

2. Cerebral aspergillosis

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91
Q

Encephalitis - Non infectious causes:

A
  1. Metabolic encephalopathies.

2. T-cell lymphoma.

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92
Q

Encephalitis - Risk factors:

A
  1. AIDS - toxoplasmosis when CD4 is <200.
  2. Other forms of immunosuppression.
  3. Travel in underdeveloped countries.
  4. Exposure to insect (eg mosquito) vector in endemic areas.
  5. Exposure to certain wild animals (bats) in an endemic area for rabies.
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93
Q

Encephalitis - Overall mortality:

A

About 10%.

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94
Q

Encephalitis - Clinical features:

A
  1. Patients often have a prodrome of headache, malaise, and myalgias.
  2. Within hours to days, patients become more acutely ill.
  3. Patients frequently have signs and symptoms of meningitis (headache, fever, photophobia, nuchal rigidity).
  4. Altered sensorium, possibly including confusion, delirium, disorientation, and behavior abnormalities.
  5. Focal neurologic findings - Hemiparesis, aphasia, cranial nerve lesions, seizures.
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95
Q

Encephalitis - Diagnosis:

A
  1. Routine lab tests - to rule out viral causes. Include CXR, urine and blood cultures, urine tox screen, and serum chemistries.
  2. Perform LP –> Examine CSF.
  3. MRI of the brain –> IMAGING STUDY OF CHOICE.
  4. EEG –> Helpful in diagnosing HSV-1.
  5. Brain biopsy –> In an acutely ill patient with a focal, enhancing lesion on MRI without a clear diagnosis.
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96
Q

Encephalitis - Management of possible complications:

A
  1. Seizures - require anticonvulsant therapy.

2. Cerebral edema - Treatment may include hyperventilation, osmotic diuresis, and steroids.

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97
Q

DDX in patients with fever + altered mental status:

A
  1. Infection –> Sepsis, UTI/urosepsis, pneumonia, bacterial meningitis, intracranial abscess, subdural empyema.
  2. Medication/drugs –> Neuroleptic malignant syndrome (haloperidol, phenothiazines).
  3. Delirium tremens.
  4. Metabolic –> Thyroid storm.
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98
Q

Hepatitis in immunosuppressed:

A

By CMV, EBV, HSV.

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99
Q

Hep B is associated with…?

A

PAN

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100
Q

Hep C is associated with…?

A

Cryoglobulinemia

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101
Q

Course of hep B - Acute infection subclinical in?

A

70%.

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102
Q

Course of hep B:

A

Resolution –> 90%.
Chronic hep –> 5-10%.
Chronic carrier –> <1%.

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103
Q

Course of CHRONIC hep B:

A

Cirrhosis –> In 25%, 10-30yrs after onset.

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104
Q

HCC from hep B infection:

A
  1. Chronic hep (5-10%).

2. Chronic carrier (<5%).

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105
Q

Course of hep C - Acute infection subclinical in?

A

75%

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106
Q

Course of hep C:

A

Chronic hep –> 85-90%.
Resolution –> 10-15%.
Fulminant –> <1%.

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107
Q

Course of CHRONIC hep C:

A

Cirrhosis –> In 10-20% of all patients - 20-30yrs after onset.

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108
Q

Hep E is particularly prevalent in:

A
  1. India
  2. Pakistan
  3. Southeast Asia
  4. Parts of Africa.
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109
Q

If transaminases are markedly elevated (>500), think:

A
  1. Acute viral hepatitis.
  2. Shock liver.
  3. Drug-induced hepatitis.
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110
Q

Risk of developing cirrhosis or HCC in chronic hep B:

A

25-40%.

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111
Q

Risk of developing cirrhosis or HCC in chronic HCV:

A

10-25%.

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112
Q

In acute hep or in drug-induced hep is ALT more elevated?

A

In acute hep.

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113
Q

In chronic HBV or in chronic HCV is ALT higher?

A

In chronic HBV, but it varies.

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114
Q

Hep and Hep B treatment:

A

Active (vaccine) and passive (Ig) immunization are available for BOTH.

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115
Q

Chronic hep B Treatment:

A
  1. IFN-alpha.

2. Lamivudine (nucleoside analog).

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116
Q

Chronic HCV treatment:

A
  1. IFN-alpha.

2. Ribavirin

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117
Q

Botulism - General:

A
  1. Ingestion of PREFORMED TOXINS (!!!!).
  2. Toxins can be inactivated by cooking food at high temperatures.
  3. Wound contamination is another source for botulism.
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118
Q

Botulism - Severity of illness:

A

Varies widely, from mild, self-limiting symptoms, to rapidly fatal disease.

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119
Q

Botulism - Clinical features:

A
  1. Abdominal cramps.
  2. Nausea.
  3. Vomiting.
  4. Diarrhea.
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120
Q

Botulism - Hallmark:

A

Symmetric, DESCENDING flaccid paralysis.

Starts with dry mouth, diplopia, and/or dysarthria. Paralysis of limb musculature occurs later.

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121
Q

Botulism - Diagnosis:

A
  1. DEFINITIVE diagnosis is IDENTIFICATION of toxin in serum, stool, or gastric contents (bioassay).
  2. Identifying C.botulinum alone in food is NOT a reliable diagnostic indicator.
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122
Q

Botulism - Treatment:

A
  1. Admit patient and observe respiratory status closely. Gastric laavge is helpful only within several hrs after ingestion of suspected food.
  2. If suspicion is high, administer antitoxin (toxoid) as soon as lab specimens are obtained (do NOT WAIT for the results).
  3. For contaminated wounds - Wound cleansing and penicillin.
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123
Q

DDX of food-borne botulism:

A
  1. Guillain-Barre syndrome - Characteristically ASCENDING paralysis, but ONE VARIETY (Fischer) can be DESCENDING.
  2. Eaton-Lambert syndrome.
  3. Myasthenia gravis - EMG studies differentiate.
  4. Diphtheria.
  5. Tick paralysis.
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124
Q

Intra-abdominal abscess - Etiology:

A
  1. Spontaneous bacterial peritonitis.
  2. Pelvic infection (eg tubo-ovarian abscess).
  3. Pancreatitis
  4. Perforation of the GI.
  5. Osteomyelitis of the vertebral bodies with extension into the retroperitoneal cavity.
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125
Q

Intra-abdominal abscess - Diagnosis:

A

CT or US.

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126
Q

Intra-abdominal abscess - Treatment:

A
  1. Typically involves DRAINAGE of the abscess.

2. Antibiotic regimen should include broad coverage against Gram(-) rods, enterococci, and anaerobes.

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127
Q

Non infectious causes of cystitis or cystitis-like symptoms:

A
  1. Cytotoxic agents (eg cyclophosphamide).
  2. Radiation to pelvis.
  3. Dysfunctional voiding.
  4. Interstitial cystitis.
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128
Q

Host-dependent factors - Incr. risk for recurrent or complicated UTIs:

A
  1. DM - Incr. risk for recurrent UTIs.
  2. Patients with spinal cord injury.
  3. Immunocompromised.
  4. Any structural/functional abnormality that impedes urinary flow (eg incomplete voiding, neurogenic bladder, BPH, vesicourethral reflux, calculi).
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129
Q

Male risk factors - UTIs:

A
  1. Uncircumsized males are at higher risk due to bacterial colonization of the foreskin.
  2. Anal intercourse.
  3. Vaginal intercourse with a female colonized with uropathogens.
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130
Q

Lower UTIs - When to obtain cultures:

A
  1. Age >65.
  2. Diabetes.
  3. Recurrent UTIs.
  4. Presence of symptoms for 7days or more.
  5. Use of a diaphragm.
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131
Q

Major clinical feature to remember about LOWER UTIs:

A

In LOWER UTIs, fever is characteristically ABSENT.

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132
Q

Asymptomatic bacteriuria - Diagnosis:

A

2 successive positive cultures (>10^5CFU/mL) must be present.

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133
Q

Asymptomatic bacteriuria - Treat when?

A

Only in pregnancy or before urologic surgery.

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134
Q

Lower UTIs - Diagnosis - Dipstick analysis:

A
  1. Leukocyte esterase test (+) –> Pyuria.

2. Positive nitrite test for presence of bacteria (gram(-)) –> Sensitive for Enterobacteriaceae.

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135
Q

Urinalysis - Most important finding:

A

Presence of WBCs.

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136
Q

Urinalysis - Adequacy of collection:

A
  1. Presence of epithelial (squamous) cells indicates vulvar or urethral contamination.
  2. If contamination is suspected, perform a straight catheterization of the bladder.
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137
Q

Urinalysis - Criteria for UTI - Bacteriuria:

A

> 1 organism per oil-immersion field.

Bacteriuria without WBCs may reflect contamination and is NOT a reliable indicator of infection.

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138
Q

Urinalysis - Criteria for UTI - Pyuria:

A

It is the most valuable finding for diagnosis: Greater than or equal to 10 leukocytes/μL is ABNORMAL.

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139
Q

Urinalysis - Other findings:

A

Hematuria and mild proteinuria may be present. Hematuria in and of itself does NOT require extended therapy.

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140
Q

Lower UTIs - Diagnosis - Urine culture:

A
  1. Confirms the diagnosis (high specificity).
  2. Traditional criteria –> >10^5 CFU/mL –> misses up to 1/3 of UTIs.
  3. Colony counts as low as 10^2 to 10^4 CFU/mL are adequate for diagnosis if clinical symptoms are present.
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141
Q

Lower UTIs - Diagnosis - Blood culture:

A

Only indicated if patient is ill and urosepsis is suspected.

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142
Q

Complicated UTI:

A
  1. Any UTI that spreads beyond the bladder (eg pyelonephritis, prostatitis, urosepsis) –> Risk factors for upper UTI: pregnancy, diabetes, and vesicoureteral reflux.
  2. Any UTI caused by structural abnormalities, metabolic disorder, or neurologic dysfunction.
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143
Q

Complications - UTI during pregnancy:

A

Incr. risk of preterm labor, low birth weight, and other complications, especially in advanced pregnancy.

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144
Q

Complications - Recurrent infections:

A
  1. Usually due to infection with new organism, but sometimes is a relapse due to unsuccessful treatment of the original organism.
  2. Risk factors include impaired host defenses, pregnancy, vesicourethral reflux, and sexual intercourse in women.
  3. Generally the consequences are not significant unless the patient is at risk for upper UTI.
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145
Q

The following groups are considered to have complicated UTI:

A
  1. Men
  2. Diabetics
  3. Renal failure
  4. Pregnancy
  5. History of pyelonephritis in last year
  6. UT obstruction, indwelling catheter, stent, nephrostomy tube.
  7. Antibiotic resistant organism .
  8. Immunocompromised patients (HIV, transplant patients).
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146
Q

UTIs treatment - For uncomplicated UTI:

A

Empiric treatment is appropriate - do NOT wait for culture results.
If complicated EXTEND TREATMENT TO 7DAYS.

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147
Q

UTI treatment - Pregnant women with UTI:

A
  1. Treat with ampicillin, amoxicillin, or oral cephalosporins for 7-10days.
  2. Avoid fluoroquinolones (can cause fetal arthropathy(!)).
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148
Q

UTI treatment - UTIs in men:

A
  1. Treat as uncomplicated cystitis in women, but for 7 days.

2. Perform a urologic workup if there are complications or recurrences, or if initial treatment fails.

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149
Q

UTI treatment - Recurrent infections:

A
  1. If a relapse occurs within 2 weeks of cessation of treatment, continue treatment for 2 more weeks and obtain a urine culture.
  2. Otherwise treat as for uncomplicated cystitis. If the patient has more than two UTIs per year, give chemoprophylaxis.
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150
Q

Pyelonephritis - Complications (unusual):

A
  1. Sepsis occurs in 10-25% of patients with pyelonephritis. May lead to shock(!).
  2. Emphysematous pyelonephritis - caused by gas-producing bacteria in diabetic patients.
  3. Chronic pyelonephritis and scarring of the kidneys - rare unless underlying renal disease exists.
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151
Q

Pyelonephritis - Diagnosis - Urinalysis:

A
  1. Look for pyuria, bacteriuria, and leukocyte casts.

2. As in cystitis, hematuria and mild proteinuria may be present.

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152
Q

Pyelonephritis - Diagnosis - Blood/urine cultures:

A

Blood cultures –> Obtain in ill-appearing patients and ALL hospitalized patients.
Urine cultures –> Obtain in ALL patients with suspected pyelonephritis.

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153
Q

Pyelonephritis - Diagnosis - CBC:

A

Leukocytosis with left shift.

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154
Q

Pyelonephritis - Diagnosis - Renal function:

A

This is usually preserved. Impairment is usually reversible, especially with IV fluids.

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155
Q

Pyelonephritis - Diagnosis - Imaging studies:

A

Perform these if treatment fails or in any patient with complicated pyelonephritis. Consider renal US, CT, IVP, or retrograde ureterogram.

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156
Q

Treatment for uncomplicated pyelonephritis:

A
  1. Use outpatient treatment if the patient can take ORAL antibiotics. Treat based on gram stain.
  2. Repeat urine culture 2-4 days after cessation of therapy.
  3. If symptoms fail to resolve within 48hr, adjust treatment based on urine culture.
  4. Further failure to respond –> Urologic investigation.
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157
Q

For recurrent pyelonephritis:

A
  1. If relapse is due to the same organism despite appropriate treatment, treat for 6 weeks.
  2. If relapse is due to a new organism, treat with appropriate therapy for 2 weeks.
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158
Q

Prostatitis - Acute or chronic bacterial is more common?

A

Chronic bacterial is more common.

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159
Q

Acute bacterial prostatitis occurs more commonly in?

A

Younger men.

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160
Q

Prostatitis - Pathophysiology:

A
  1. Ascending infection.
  2. May occur after catheterization.
  3. Other causes - direct/lymphatic spread from the rectum.
  4. Hematogenous spread (rare).
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161
Q

Acute bacterial prostatitis - Causative organisms:

A

Gram(-) organisms predominate - E.coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Serratia spp.

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162
Q

Chronic bacterial prostatitis - Prevalence:

A

True prevalence is difficult to determine because many cases are asymptomatic and are diagnosed incidentally.

163
Q

Chronic bacterial prostatitis - Target:

A

40-70yrs.

164
Q

Chronic bacterial prostatitis - Causative organisms:

A

Similar to acute bacterial prostatitis - Can occur from chronic prostatitis.

165
Q

Acute or chronic bacterial prostatitis is a more serious condition:

A

Acute.

166
Q

Acute prostatitis - Clinical features:

A
  1. Fevers, chills - Patients may appear toxic(!).
  2. Irritative voiding symptoms - Dysuria, frequency, urgency.
  3. Perineal pain, low back pain, urinary retention may be present as well.
167
Q

Prostatic massage in patients with acute bacterial prostatitis may cause:

A

Bacteremia. SKIP RECTAL EXAM if the diagnosis is straightforward, given the risk of inducing bacteremia.

168
Q

Chronic bacterial prostatitis - Clinical features:

A
  1. Patients may be asymptomatic. Patients do no appear ill. Fever is uncommon.
  2. Patients frequently have recurrent UTIs with irritative voiding and/or obstructive symptoms.
  3. There is a dull, poorly localized pain in the lower back, perineal, scrotal, or suprapubic region.
169
Q

Prostatitis - Diagnosis:

A
  1. DRE - Acute: boggy, exquisitely tender prostate. Chronic: enlarged and usually non tender.
  2. Urinalysis - Numerous WBCs (!) in ACUTE prostatitis.
  3. Urine cultures - Almost always positive in acute prostatitis.
  4. Chronic prostatitis - Presence of WBCs in expressed prostatic secretions suggests diagnosis. Urine cultures may be positive (chronic bacterial prostatitis) or negative (non bacterial prostatitis).
170
Q

Acute prostatitis - Treatment:

A
  1. If it is SEVERE and the patient appears TOXIC, hospitalize the patient and initiate IV antibiotics.
  2. If is it MILD, treat on an outpatient basis with antibiotics - TMP/SMX or a fluoroquinolone and doxycycline. Treat for 4-6 weeks.
  3. Patients usually responds to therapy.
171
Q

Chronic prostatitis - Treatment:

A
  1. Fluoroquinolone. Prolonged course is recommended but DOES NOT guarantee complete eradication.
  2. It is very difficult to treat. Recurrences are common.
172
Q

MC STD:

A

Genital warts - Associated with HPV.

173
Q

80% of cases of Reiter’s syndrome are associated with?

A

Chlamydial infection.

174
Q

MC BACTERIAL STD:

A

Chlamydial infection - Many are co-infected with gonorrhea (up to 40% of women and 20% of men.

175
Q

Chlamydial incubation period:

A

1-3wks.

176
Q

Chlamydial infection is a risk factor for…?

A

Cervical cancer, especially when there is a history of multiple infection.

177
Q

Chlamydia - Clinical features:

A
  1. Many cases are asymptomatic (80% of women, 50% of men).
  2. MEN who are symptomatic may have any of the following: dysuria, purulent urethral discharge, scrotal pain and swelling, and fever.
  3. WOMEN who are symptomatic may have purulent urethral discharge, intermenstrual or post coital bleeding, and dysuria.
178
Q

Complications of chlamydia:

A
  1. MEN –> Epididymitis and proctitis.
  2. WOMEN –> PID, salpingitis, tubo-ovarian abscess, ectopic pregnancy, Fitz-Hugh-Curtis syndrome.
    - -> Leading cause of infertility in women due to tubal scarring.
179
Q

Chlamydia - Diagnosis:

A
  1. Culture, enzyme immunoassay, and molecular tests such as PCR. NOT serology(!).
  2. PCR replaces culture as the screening test of choice due to higher sensitivity.
  3. Sexually active adolescents (particularly females) should be screened for chlamydial infection even if they are asymptomatic.
180
Q

Chlamydial - Treatment:

A
  1. Azithromycin (oral 1 dose) or doxycyclin (oral for 7 days).
  2. Treat all sexual partners.
181
Q

Gonorrhea is usually symptomatic in…?

A

Men.

THEREFORE –> Complications occur more often in women due to undetected disease.

182
Q

What other sites besides the genitalia can gonorrhea infect?

A
  1. Pharynx
  2. Conjunctiva
  3. Rectum
183
Q

Gonorrhea transmission:

A
  1. Sexually

2. Neonatally

184
Q

Gonorrheal complications (more often seen in women):

A
  1. PID - possible infertility, chronic pelvic pain.
  2. Epididymitis, prostatitis (uncommon).
  3. Salpingitis, tubo-ovarian abscess.
  4. Fitz-Hugh-Curtis syndrome (perihepatitis) - RUQ pain; elevated LFTs.
  5. Disseminated gonococcal infection.
185
Q

Gonorrhea - Clinical features - Men:

A
  1. Gonorrhea is asymptomatic in up to 10% of carriers. These can STILL transmit the disease.
  2. Most men have symptoms involving the urethra - eg purulent discharge, dysuria, erythema, edema of urethral meatus, frequency of urination.
186
Q

Gonorrhea - Clinical features - Women:

A

Most women are asymptomatic or have a few symptoms(!).

May have symptoms of cervicits/urethritis - eg purulent discharge, dysuria, intermenstrual bleeding, and dyspareunia.

187
Q

Disseminated gonococcal infection - Clinical findings:

A

Occurs in 1%-2% of cases; more common in WOMEN:

  1. Fever, arthralgias, tenosynovitis (of hands and feet).
  2. Migratory polyarthritis/septic arthritis, endocarditis, or even meningitis.
  3. Skin rash (usually on distal extremities).
188
Q

Gonorrhea - Diagnosis:

A
  1. Gram stain of urethral discharge showing organisms WITHIN leukocytes is highly SPECIFIC for gonorrhea.
  2. Obtain cultures in ALL CASES - May treat empirically because culture results take 1-2 days to return.
  3. Consider testing for syphilis and HIV(!).
  4. Obtain BLOOD CULTURES if disease has disseminated.
189
Q

Gonorrhea - Treatment:

A
  1. Ceftriaxone (IM, 1dose) –> also effective against syphilis.
  2. Other: Cefixime, ciprofloxacin, ofloxacin.
  3. Also give azithromycin (one dose) or doxycycline (for 7 days) to cover COEXISTENT chlamydial infection.
  4. If disseminated, hospitalize the patient and initiate ceftriaxone (IV or IM for 7 days).
190
Q

Why is it important, but often difficult, to identify patients with primary HIV infection?

A

Because of the benefits of EARLY antiretroviral therapy - High index of suspicion is necessary.

191
Q

HIV transmission:

A
  1. Sexually
  2. Parenterally
  3. Via semen
  4. Blood
  5. Fluids
  6. Breast milk
  7. Vaginal fluid
192
Q

Risk of HIV transmission - Needlestick injury:

A

1/300

193
Q

Risk of HIV transmission - Vaginal (male to female):

A

1/1.000

194
Q

Risk of HIV transmission - Vaginal (female to male):

A

1/3.000

195
Q

Risk of HIV transmission - Anal receptive:

A

1/100

196
Q

Risk of HIV transmission - Mother to child:

A

With medications –> 2/100.

Without medications –> 1/3.

197
Q

Caesarian delivery is indicated if viral load is over?

A

1.000 copies.

198
Q

Caesarian section is NOT indicated in an HIV(+) mother when…?

A

CD4>500

Viral load <1.000

199
Q

4 phases of typical HIV course:

A
  1. Primary infection.
  2. Asymptomatic infection.
  3. Symptomatic infection.
  4. Full-blown AIDS.
200
Q

Pre-AIDS phase (symptomatic HIV infection):

A
  1. 1st evidence of immune system dysfunction.
  2. Without treatment this phase lasts about 1-3yrs.
  3. The following frequently appear:
    a. Persistent generalized lymphadenopathy.
    b. Localized fungal infections (eg on fingernails, toes, mouth).
    c. Recalcitrant vaginal yeast and trichomonal infections in women.
    d. Oral hairy leukoplakia on the tongue.
    e. Skin manifestations that include seborrheic dermatitis, psoriasis exacerbations, molluscum, warts.
201
Q

What is used to indicate when to initiate antiretroviral therapy and PCP prophylaxis?

A

CD4 count - Also useful in assessing response to therapy.

202
Q

If untreated (no retroviral therapy), CD4 count decreases at an average rate of about…?

A

50 cells per YEAR.

203
Q

HIV viral load - Importance:

A

Used to assess response to and adequacy of antiretroviral therapy. Provides complementary prognostic information to the CD4 count.

204
Q

HIV - Diagnosis - PCR:

A

PCR RNA viral load test –> Patients with ACUTE HIV infection have very high levels of viremia - This test is repeated to assess effectiveness of therapy.

205
Q

HIV - Diagnosis - p24 antigen assay:

A

Less costly but less sensitive alternative to viral loading testing.

206
Q

HIV seroconversion occurs in…?

A

3-7WEEKS.

207
Q

HIV - Diagnosis - ELISA:

A

Screening test for detecting antibody to HIV - Becomes positive 1-12 weeks after infection.
A negative ELISA essentially EXCLUDES HIV (99% sensitive) as long as the patient has not had a subsequent exposure before testing (before seroconversion).

208
Q

Diagnosis of AIDS:

A
  1. Depends principally on the identification of an indicator condition or on finding in an HIV-1 seropositive patient with a CD4 cell count lower than 200.
  2. There are many indicator conditions (AIDS-defining illnesses).
209
Q

Antiretroviral therapy in HIV:

A

The importance of strict (100%) adherence to the triple-drug regimen CANNOT BE OVEREMPHASIZED, because even minor deviations may result in drug resistance.
–> Do NOT initiate triple-drug therapy in a patient who is NOT willing or able to fully comply with the prescribed regimen.

210
Q

Antiretroviral therapy - Indications:

A
  1. Symptomatic patients regardless of CD4 count.

2. Asymptomatic patients with CD4 count <500.

211
Q

HAART consists of:

A

2 NucleoSide reverse transcriptase inhibitors and either:

  • A NON nucleoside reverse transcriptase inhibitor.
  • A PI.
212
Q

HAART in pregnant women?

A

Generally recommended to be continued in pregnancy.

213
Q

Opportunistic infection prophylaxis - Tests:

A
  1. CXR (bilateral interstitial infiltrates).
  2. LDL level (always elevated).
  3. ABG (hypoxia or incr. A-a gradient).
  4. Sputum stain for pneumocystis (very specific but not sensitive).
  5. Bronchoscopy with bronchoalveolar lavage (most accurate test).
214
Q

Opportunistic infection prophylaxis - Preferred agent:

A

TMP-SMX.

215
Q

HIV(+) - TB treatment:

A
  1. Screen all patients with a yearly PPD test.

2. Prescribe INH + pyridoxine if the patient has positive PPD.

216
Q

Opportunistic infection prophylaxis - Atypical mycobacteria?

A
  1. Start prophylaxis when CD4<100.

2. Clarithro/Azithro.

217
Q

Opportunistic infection prophylaxis - Toxoplasmosis:

A
  1. Give this to patients with CD4<100.

2. TMP/SMX.

218
Q

Opportunistic infection prophylaxis - Vaccination:

A

NO LIVE-VIRUS VACCINES.

  1. Pneumococcal polysaccharide vaccine (Pneumovax) - Every 5-6 YEARS.
  2. Influenza vaccine - Yearly.
  3. Hep B vaccine (if not already antibody positive).
219
Q

HSV - Pathophysiology:

A
  1. After inoculation, the HSV replicates in the DERMIS and EPIDERMIS.
  2. Then travels via sensory nerves up to the dorsal root ganglia.
  3. It resides as a latent infection in the dorsal root ganglia.
  4. Where it can be reactivated at any time and reach the skin through peripheral nerves.
220
Q

HSV - Transmission:

A
  1. Transmitted by contact with people who have active ulcerations or shedding of virus from mucous membranes.
  2. HSV-1 is typically associated with transmission through NON sexual personal contact (eg kissing), and HSV-2 through kissing.
221
Q

Contracting one form of herpes confers some degree of…?

A

CROSS-immunity, rendering primary infection with the other form of herpes less sever.

222
Q

Infection with genital herpes is associated with an increased risk of contracting…?

A

HIV.

223
Q

HSV-1 - Oral lesions:

A

Involve group of vesicles on patches of erythematous skin.

–> Herpes labialis (cold sores) are MC on the lips (usually painful, heal in 2-6WEEKS).

224
Q

HSV-1 is associated with what palsy?

A

Bell’s palsy.

225
Q

Recurrences of HSV - Associated with:

A
  1. Stress
  2. Fever
  3. Sun exposure
  4. Infection
    - -> Tend to be shorter and less frequent over time.
226
Q

HSV-2 - Primary infection:

A

More severe + prolonged symptoms, lasting up to 3 weeks.

227
Q

HSV-2 presents with:

A
  1. Painful genital vesicles or pustules.
  2. Tender inguinal lymphadenopathy.
  3. Vaginal and/or urethral discharge.
228
Q

Disseminated HSV - Usually seen in?

A

Immunocompromised.

229
Q

Disseminated HSV - May result in?

A
  1. Encephalitis
  2. Meningitis
  3. Keratitis
  4. Chorioretinitis
  5. Pneumonitis
  6. Esophagitis
230
Q

Neonatal HSV - Features:

A
  1. Congenital malformations.
  2. Intrauterine growth retardation.
  3. Chorioamnionitis.
  4. Neonatal death.
231
Q

HSV and ocular disease?

A

EITHER form of HSV can cause ocular disease.

232
Q

Herpetic whitlow:

A
  1. HSV infection of the finger caused by inoculation into open skin surface - Common in health care workers.
  2. Painful vesicular lesions erupt in fingertip.
  3. May cause fever + axillary lymphadenopathy.
  4. Treat with acyclovir.
    - -> DO NOT mistake for PARONYCHIA - Incision and drainage should NOT be done for herpetic whitlow.
233
Q

HSV - Diagnosis:

A
  1. Can be made clinically when characteristic lesions are recognized.
  2. If there is uncertainty, perform:
    a. Tzanck smear - quickest test.
    b. Culture of HSV (gold standard).
    c. ELISA.
234
Q

Tzanck smear:

A
  1. Perform by swabbing the base of the ulcer and staining with Wright’s stain.
  2. Shows multinucleated giant cells. Does NOT differentiate between HSV and VZV.
235
Q

Culture of HSV:

A
  1. Perform by swabbing the base of the ulcer.

2. Results are available within 2-3 days.

236
Q

ELISA for HSV:

A
  1. 80% sensitive.

2. Results available within MINUTES to HOURS.

237
Q

Syphilis - Transmission:

A

Direct sexual contact with infectious lesions.

238
Q

MC presentations for syphilis:

A
  1. Genital lesions (chancre).
  2. Inguinal lymphadenopathy.
  3. Maculopapular rash of secondary syphilis.
239
Q

Syphilis chancre appears when?

A

3-4 weeks after exposure.

240
Q

Syphilis chancre heals when?

A

In 14weeks, even without therapy.

241
Q

Secondary stage of syphilis - When?

A

May develop 4-8 weeks AFTER the chancre has healed.

242
Q

Secondary syphilis - Most characteristic finding:

A

Maculopapular rash.

243
Q

Latent syphilis - Definition:

A

Presence of positive serologic test results in the ABSENCE of clinical signs or symptoms.
1/3 develops tertiary syphilis.

244
Q

Early and late tertiary syphilis:

A

Early –> If serology has been positive for Patient may relapse back to secondary syphilis.
Late –> If serology has been positive for >1yr –> Not contagious during this time, none of the symptoms are present.

245
Q

Syphilis - Diagnosis - Definitive diagnostic test:

A

Dark-field microscopy - examines a sample of the chancre with visualization of spirochetes.

246
Q

Diagnosis of syphilis - Steps:

A
  1. Obtain VDLR + RPR.

2. IF POSITIVE –> Confirm with FTA-ABS.

247
Q

Diagnosis of syphilis - Non treponemal tests:

A

RPR and VDRL (most commonly used) –> Ideal for screening.

248
Q

Diagnosis of syphilis - Treponemal tests:

A

FTA-ABS, MHA-TP –> For confirmation.

249
Q

Diagnosis of syphilis - ALL PATIENTS should ALSO be tested for?

A

HIV infection.

250
Q

Treatment of syphilis:

A 
Benzathine penicillin (IM, 1 dose).
If allergic --> Doxycycline, tetracycline for 2 WEEKS(!).
251
Q

Treatment of late latent syphilis or tertiary syphilis?

A

Give penicillin in 3 doses IM once PER WEEK.

252
Q

Treatment of syphilis - How to ensure adequate response?

A

Repeat non treponemal tests every 3 months. Titers should decrease 4-fold within 6 months.
–> If they do NOT, that may signal treatment failure or reinfection.

253
Q

RPR and VDLR may be falsely positive in…?

A

SLE(!).

254
Q

Chancroid - Caused by?

A

H.ducreyi - Gram(-) rod.

255
Q

Chancroid - Transmission:

A

Sexually

256
Q

Incubation period of H.ducreyi:

A

2-10days.

257
Q

Diagnosis of chancroid:

A

It is made CLINICALLY:

  1. Painful genital ulcer (s).
  2. Tender lymphadenopathy.
  3. Syphilis RULED OUT (negative dark-field exam + negative serology).
  4. HSV RULED OUT based on clinical presentation or negative culture for HSV.
258
Q

Chancroid - Treatment options:

A
  1. Azithromycin (oral, 1 dose).
  2. Ceftriaxone (IM, 1 dose).
  3. Oral course of azithromycin, erythromycin, ciprofloxacin.
    - -> With treatment –> Most ulcers resolve in 1 or 2 weeks.
259
Q

Lymphogranuloma venereum - Features:

A
  1. PainLESS ulcer at the site of inoculation that may go unnoticed.
  2. FEW WEEKS later –> tender inguinal lymphadenopathy (usually unilateral) and constitutional symptoms develop.
260
Q

Lymphogranuloma venereum - If untreated?

A

Proctocolitis may develop with perianal fissures and rectal stricture.
–> Obstruction of lymphatics may lead to elephantiasis of genitals.

261
Q

Lymphogranuloma venereum - Diagnosis:

A

Serology - complement fixation, immunofluorescence.

–> Treatment is doxycycline - oral for 21days.

262
Q

3 forms of pediculosis:

A
  1. Pediculosis capitis (head lice).
  2. Pediculosis corpora (body lice).
  3. Pediculosis pubis (pubic lice or “crabs”).
263
Q

Pediculosis pubis - What is it?

A

A common STD caused by Phthirus pubis (the pubic or crab louse).

264
Q

Phthirus pubis - Transmission:

A

Sexually, via clothes, or towels.

265
Q

Pediculosis pubis - Main features:

A

SEVERE PRURITUS in the genital region is characteristic. Other hairy areas of the body may be involved.

266
Q

Pediculosis pubis - Diagnosis:

A

Made by examination of hair under microscope (or possibly with the naked eye) - identification of adult lice or nits.

267
Q

Pediculosis pubis - Treatment:

A

Permethrin 1% shampoo (Elimite).

268
Q

Cellulitis is?

A

An inflammatory condition of skin + subcutaneous tissue.

269
Q

Cellulitis is caused by?

A

A wide variety of bacteria, MC being group A streptococci or S.aureus.

270
Q

Cellulitis - If untreated?

A

Cellulitis may lead to potentially life-threatening bacteremia.

271
Q

Cellulitis - Fever?

A

May or may NOT be present.

272
Q

Cellulitis - recurrences in the same area?

A

Patients with cellulitis are predisposed to recurrences in the SAME AREA because of damage that occurs to the LOCAL LYMPHATIC vessels.

273
Q

Cellulitis - Diagnosis:

A
  1. Essentially clinical.
  2. Obtain blood cultures if the patient has fever.
  3. Obtain tissue cultures if there is a wound, ulcer, or site of infection.
  4. Obtain imaging (plain film, MRI) if there is suspicion of deeper infection.
274
Q

Cellulitis - Treatment:

A
  1. Base treatment on suspected pathogens from the patients history. Most patients require PARENTERAL antibiotic therapy.
  2. Treat with a staph penicillin (oxacillin, nafcillin) or a cephalosporin (cefazolin).
  3. Continue IV antibiotics until signs of infection improve –> Follow up with oral antibiotics for 2 weeks.
275
Q

Erysipelas is a…?

A

Cellulitis that is usually confined to the dermis and lymphatics.

276
Q

Erysipelas - Cause:

A

Usually caused by group A strep.

277
Q

Erysipelas - Predisposing factors:

A
  1. Lymphatic obstruction (radical mastectomy).
  2. Local trauma or abscess.
  3. Fungal infections.
  4. DM.
  5. Alcoholism.
278
Q

Erysipelas - Complications:

A
  1. Sepsis.
  2. Local spread to subcutaneous tissues.
  3. Necrotizing fasciitis.
279
Q

Erysipelas - Treatment:

A

For UNcomplicated cases is IM or oral penicillin or erythromycin - Otherwise treat as for cellulitis.

280
Q

Erysipelas has a high rate of…?

A

Recurrences.

281
Q

Common pathogens in cellulitis - Local trauma, breaks in skin:

A

Group A strep (pyogenes).

282
Q

Common pathogens in cellulitis - Wounds, abscesses:

A

S.aureus.

283
Q

Common pathogens in cellulitis - Immersion in water:

A
  1. P.aeruginosa
  2. Aeromonas hydrophila
  3. Vibrio vulnificus
284
Q

Common pathogens in cellulitis - Acute sinusitis:

A

H.influenza.

285
Q

Necrotizing fasciitis is…?

A

A life-threatening infection of deep soft tissues that rapidly tracks along facial planes.

286
Q

Necrotizing fasciitis - Causes:

A

S.pyogenes (Group A) and C.perfringens.

287
Q

Necrotizing fasciitis - Risk factors:

A
  1. Recent surgery.
  2. Diabetes.
  3. Trauma.
  4. IVDA.
288
Q

Necrotizing fasciitis - Clinical features:

A
  1. Fever + Pain OUT OF PROPORTION of appearance of skin in early stages, so a high index of suspicion is important.
  2. Extension of infection leads to thrombosis of microcirculation –> tissue necrosis, discoloration, crepitus, and cutaneous anesthesia.
289
Q

Necrotizing fasciitis may rapidly progress to…?

A

Sepsis, TSS, and multi-organ failure.

290
Q

Necrotizing fasciitis - Treatment:

A
  1. Antibacterial treatment alone is NOT sufficient.
  2. Rapid SURGICAL exploration and excision of devitalized tissue is an absolute necessity!!!.
  3. Broad-spectrum parenteral antimicrobial therapy is warranted.
291
Q

Differentiating DVT from cellulitis:

A
  1. Like cellulitis, acute DVT ALSO presents with erythema, warmth, and tenderness in the affected extremity.
  2. Inflammation in DVT is usually restricted to the posterior calf.
  3. Because Homans’ sign and the palpation of venous cords are NOT sensitive in detecting DVT, VENOUS DOPPLER must sometimes be performed to differentiate between cellulitis and acute DVT.
292
Q

Lymphadenitis - Often caused by?

A

Local skin or soft tissue bacterial infection - often hemolytic streptococci and staph.

293
Q

Lymphadenitis - Presentation:

A
  1. Fever.
  2. Tender lymphadenopathy of regional lymph nodes.
  3. Red streaking of skin from the wound or area of cellulitis.
294
Q

Lymphadenitis - Complications:

A
  1. Thrombosis of adjacent veins.
  2. Sepsis.
  3. Even death if untreated.
295
Q

Lymphadenitis - Diagnosis:

A

Helpful diagnostic studies include BLOOD and WOUND cultures.

296
Q

The following types of wounds are most likely to result in tetanus:

A
  1. Wounds contaminated with dirt, feces, or saliva.
  2. Wounds with necrotic tissue.
  3. Deep-puncture wounds.
297
Q

Incubation period for tetanus ranges from about?

A

2 days to 2 weeks. (GRADUAL onset 1 to 7 days)

298
Q

Tetanus - Clinical features - Classic and earliest symptom:

A

Classic and earliest symptom is hypertonicity and contractions of the masseter muscles, resulting in trismus, or “lockjaw

299
Q

Tetanus - Clinical features - Progression:

A

Generalized muscle contractions including:
a. Risus sardonicus - grin due to contraction of facial muscles.
b. Opisthotonus - arched back due to contraction of back muscles.
+ Sympathetic hyperactivity.

300
Q

Tetanus - Diagnosis:

A
  1. Mainly clinical.

2. Obtain wound cultures, but they are NOT a reliable means of diagnosis.

301
Q

Tetanus - Treatment:

A
  1. Admit patient to the ICU and provide respiratory support if necessary. Give DIAZEPAM for tetany.
  2. Neutralize unbound toxin with passive immunization - Give a single IM dose of tetanus Ig (TIG).
  3. Provide active immunization with tetanus/diphtheria toxoid (Td).
  4. Thoroughly clean and debride any wounds with tissue necrosis.
  5. Give antibiotics (metronidazole or penicillin G), although efficacy is somewhat controversial.
302
Q

Osteomyelitis - 2 main categories:

A
  1. Hematogenous osteomyelitis (MC in children) - occurs secondary to sepsis.
  2. Direct spread of bacteria from any of the following:
    a. Adjacent infection (eg infected diabetic foot ulcer, decubitus ulcer).
    b. Trauma (eg open fractures).
    c. Vascular insufficiency (eg peripheral vascular disease).
303
Q

Osteomyelitis - Causes:

A

MC is S.aureus and CN staph.

304
Q

Osteomyelitis - Sites:

A
  1. Long bones (tibia, femur, humerus).
  2. Foot and ankle.
  3. Vertebral bodies.
305
Q

Osteomyelitis - Risk factors:

A
  1. Open fractures.
  2. DM –> Predisposition to infection and peripheral vascular disease.
  3. Use of illicit IV drugs.
  4. Sepsis.
306
Q

Osteomyelitis - MC finding:

A

Pain over the involved area.

307
Q

Osteomyelitis - Finding with chronic disease:

A

A draining sinus tract through the skin may form in chronic disease.

308
Q

Common bugs in osteomyelitis - Catheter septicemia:

A

S.aureus

309
Q

Common bugs in osteomyelitis - Prosthetic joint:

A

CN staph

310
Q

Common bugs in osteomyelitis - Diabetic foot ulcer:

A

Polymicrobial organisms.

311
Q

Common bugs in osteomyelitis - Nosocomial infections:

A

Pseudomonas spp.

312
Q

Common bugs in osteomyelitis - IVDA, neutropenia:

A

Fungal spp., Pseudomonas spp.

313
Q

Common bugs in osteomyelitis - SCA:

A

Salmonella spp.

314
Q

Up to what percentage of patients with open fractures do patients eventually develop osteomyelitis?

A

Up to 10%.

Use of orthopaedic hardware increases this risk (foreign body is the site of bacterial colonization).

315
Q

Osteomyelitis of the vertebral bodies due to M.tuberculosis is called:

A

Pott’s disease.

316
Q

Osteomyelitis - Diagnosis - WBC:

A

May or may NOT be elevated - NOT useful for diagnosis.

317
Q

Osteomyelitis - Diagnosis - Normal ESR, CPR:

A

Do NOT exclude diagnosis.

–> Useful in monitoring response to therapy.

318
Q

Osteomyelitis - Diagnosis - Most direct and accurate means of diagnosis?

A

Needle aspiration of infected bone or BONE BIOPSY (obtained in operating room).

319
Q

Osteomyelitis - Diagnosis - Plain radiography?

A

Earliest radiographic changes (periosteal thickening or elevation) are NOT evident for at least 10 DAYS.
–> Lytic lesions only in advanced disease.

320
Q

The most effective imaging study for osteomyelitis:

A

MRI - For diagnosis + Assessing the extent of disease process.

321
Q

Osteomyelitis - Treatment:

A

Give IV antibiotics for EXTENDED periods (4-6wks). Initiate antibiotic therapy only after the microbial etiology is NARROWED based on data from cultures.

322
Q

Chronic osteomyelitis refers to:

A

Bone necrosis and soft tissue compromise or to a relapse of previously treated osteomyelitis.
–> Very challenging to treat and almost impossible to completely eradicate.

323
Q

Acute infectious arthritis - Pathogenesis - Microbes penetrate via:

A
  1. Hematogenous spread - MC route.
  2. Contiguous spread from another locus of infection (eg osteomyelitis, abscess, or cellulitis).
  3. Traumatic injury to the joint.
  4. Iatrogenic (eg from arthrocentesis, arthroscopy).
324
Q

If a patient has a painless range of motion of involved joint, septic arthritis is very…?

A

Unlikely.

Micromotions of joint cause SEVERE pain in septic arthritis.

325
Q

Acute bacterial arthritis - Causative organisms:

A
  1. S.aureus is MC overall in adults + children. Also various strep spp.
  2. N.gonorrhoeae –> MCC in young, sexually active.
  3. P.aeruginosa, Salmonella spp. –> SCA, Immunodef., IVDA.
326
Q

Risk factors for acute infectious arthritis:

A
  1. Prior joint damage (eg RA).
  2. Joint prosthesis.
  3. DM.
327
Q

Acute infectious arthritis - Diagnosis - 1st step:

A

Perform a joint aspiration (“tap”) and analysis of synovial fluid in all patients suspected of having a septic joint.

328
Q

Acute infectious arthritis - Diagnosis - Studies to order on aspirated synovial fluid:

A
  1. WBC with differential - usually >50.000 WBC/mm^3 with >80% PMNs –> Most helpful test.
  2. Gram stain of fluid –> 75% is gram(+), 30-50% is gram(-).
  3. Culture - aerobic/anaerobic.
  4. Crystal analysis (!) –> Acute gout arthritis may present as septic one.
  5. PCR on synovial fluid –> If gonococcal arthritis is suspected and Gram + cultures are negative.
329
Q

Acute infectious arthritis - Diagnosis - Blood cultures:

A

Positive in >50% of all cases (frequently negative in gonoccocal arthritis).

330
Q

Acute infectious arthritis - Diagnosis - Other lab abnormalities:

A
  1. Leukocytosis - in about half of patients with a septic joint.
  2. Elevated ESR - Up to 90%.
  3. Elevated CRP - For monitoring.
331
Q

Acute infectious arthritis - Diagnosis - Imaging studies:

A
  1. Plain radiographs - Generally not useful.

2. CT or MRI - Helpful if the sacroiliac or facet joints are involved.

332
Q

Acute infectious arthritis - Treatment:

A

Prompt antibiotic treatment:

  1. Do not delay in initiating antimicrobial therapy, when acute infectious arthritis is suspected.
  2. If the Gram stain is negative, but AIA is still suspected, treat EMPIRICALLY, until culture and sensitivity results are available.
333
Q

AIA - Treatment - Drainage:

A

Daily aspiration of affected joint as long as effusion persists is one treatment option.
HOWEVER –> Surgical drainage is better.

334
Q

Complications of septic arthritis:

A
  1. Destruction of joint and surrounding structures (eg ligaments, tendons) –> Stiffness, pain, loss of function.
  2. Avascular necrosis - if hip is involved.
  3. Sepsis.
335
Q

Gonococcal arthritis - Presentation:

A
  1. Acute mono- or oligoarthritis, and often progresses within days in a migratory or additive pattern.
  2. Knees, wrists, hands, ankles are the MOST commonly involved.
  3. Tenosynovitis is often present in the hands/feet.
336
Q

Gonococcal arthritis - Signs of disseminated infection:

A
  1. Fever
  2. Chills
  3. Rash (macules, papules, and/or pustules)
    - -> Admit to the hospital.
337
Q

Septic arthritis - MC joint affected:

A

Knee.

Also –> Hip, wrist, shoulder, ankle.

338
Q

Septic arthritis in immunosuppressed or connective tissue diseases:

A

Polyarticular arthritis - and a WORSE prognosis.

339
Q

Malaria - General features - Caused by:

A 
1 of 4 organisms:
1. P.falciparum
2. P.ovale
3. P.vivax
4. P.malariae
(+knowlessi).
340
Q

Malaria - Clinical features:

A

Symptoms may include:

  1. Fever
  2. Chills
  3. Myalgias
  4. Headache
  5. Nausea
  6. Vomiting
  7. Diarrhea
341
Q

Malaria - Fever patterns:

A

P.falciparum –> Usually, constant.
P.ovale, P.vivax –> Usually, spikes every 48hrs.
P.malariae –> Usually spikes every 72hrs.

342
Q

Malaria - Onset of illness:

A

Usually occurs WEEKS to MONTHS after infection, but it is dependent on the specific cause.

343
Q

Malaria - Diagnosis:

A
  1. Identify organism on peripheral blood smear.

2. Blood smear must have Giemsa stain.

344
Q

Which microorganism is by far the most serious and life-threatening?

A

P.falciparum.

345
Q

Malaria treatment - Chloroquine resistance - What to give?

A
  1. Quinine sulfate and tetracycline.

2. Atovaquone-proguanil and mefloquine.

346
Q

P.falciparum infection may require?

A

IV quinidine + doxycycline.

347
Q

For hypnozoites in P.vivax and P.ovale infections - What to give?

A

Add a 2-week regimen of primaquine phosphate.

348
Q

Malaria prophylaxis - What to give in chloroquine resistant areas?

A

Mefloquine is the agent of choice.

349
Q

Rabies - A rare documented route of infection:

A

From a corneal transplant.

350
Q

Rabies - Incubation period:

A

Typically ranges from 30-90days, but varies considerably.

351
Q

Rabies - Symptoms in progressive order:

A
  1. Pain at the site of bite.
  2. Prodromal symptoms of sore throat, fatigue, headache, nausea, and/or vomiting.
  3. Encephalitis - Confusion, combativeness, hyperactivity, fever, seizures may be present.
  4. Hydrophobia - usually progresses to coma and death.
    - -> Some patients may present with ASCENDING paralysis.
352
Q

Rabies - Diagnosis:

A
  1. Virus or viral antigen. Virus can be isolated in saliva as well.
  2. 4-fold increase in serum antibody titers.
  3. Identification of Negri bodies histologically.
  4. PCR detection of virus RNA.
353
Q

Rabies prophylaxis:

A

Rabies vaccine is available for at-risk individuals - Those with potential occupational exposure, such as veterinarians, wild-life officials, and lab workers.

354
Q

Rabies - Treatment (post exposure management):

A
  1. Clean the wound thoroughly with soap.
  2. For wild animal bites (eg bat or raccoon), the animal should be captured if possible, destroyed, and sent to a lab for immunofluorescence of brain tissue.
  3. If the patient was bitter by a healthy dog or cat in an endemic area, the animal should be captured and observed for 10days.
355
Q

Rabies Treatment - Post exposure management - For a known rabies exposure:

A

For a known rabies, both of the following should be performed:

  1. Passive immunization - Administer human rabies Ig to patients, into the wound as well as in the gluteal region.
  2. Active immunization - Antirabies vaccines in 3 IM doses into the deltoid or thigh over a 28-day period.
356
Q

Candidiasis - Risk factors:

A
  1. Antibiotic therapy.
  2. DM.
  3. Immunosuppressive therapy.
  4. Immunocompromised hosts (incr. risk for BOTH mucocutaneous + systemic candidiasis).
357
Q

Candidiasis - Typical presentation:

A

Mucocutaneous growth.

358
Q

Candidiasis - MC affected areas:

A
  1. Vagina - yeast infection.
  2. Mouth, oropharynx - “thrush”.
  3. Cutaneous candidiasis.
  4. GI tract (esophagus).
359
Q

Candidiasis - Disseminated or invasive disease:

A

May occur in immunocompromised.

  1. Sepsis/septic shock.
  2. Meningitis.
  3. Multiple abscesses.
360
Q

Candidiasis - Diagnosis:

A
  1. Mucocutaneous candidiasis is primarily clinical; KOH preparation demostrates yeast.
  2. Invasive candidiasis is diagnosed by blood or tissue culture.
361
Q

Candidiasis - Treatment:

A
  1. Remove indwelling catheters or central lines.
  2. Acceptable treatments for oropharyngeal candidiasis –> Clotrimazole, Nystatin, Oral ketoconazole, fluconazole.
  3. Vaginal candidiasis - Miconazole or clotrimazole cream.
  4. Cutaneous candidiasis - Oral nystatin powder, keeping skin dry.
362
Q

Systemic candidiasis - Treatment:

A
  1. Amphotericin B
  2. Fluconazole.
  3. New agents –> Voriconazole and caspofungin.
363
Q

FUO - Definition:

A
  1. Fever >38.3C.
  2. Continuing “on several occasions” for at least 3 weeks.
  3. No diagnosis over this time period despite 1 week of inpatient workup.
    - -> 3 outpatient visits now substitute for 1 week in the hospital.
364
Q

FUO - Etiology:

A
  1. Infection - MCC.
  2. Occult neoplasms - 2nd MCC (lymphomas, leukemias).
  3. Collagen vascular diseases.
  4. Other causes.
365
Q

FUO - Infectious etiology:

A
  1. TB and other mycobacterial infection.
  2. Occult abscesses (eg hepatic, retroperitoneal).
  3. UTI/complicated UTI.
  4. Endocarditis.
  5. Sinusitis.
  6. HIV.
  7. Inf. mono + other viruses.
  8. Malaria and other parasitic infections.
366
Q

Persistence of fever in the ICU, despite antimicrobial therapy, should raise the index of suspicion for:

A
  1. Fungal infection.
  2. Antimicrobial resistance.
  3. Infections requiring surgical intervention (eg occult abscess, wound necrosis).
  4. Drug fever.
367
Q

FUO - Collagen vascular disease etiology:

A
  1. SLE
  2. Still’s disease (!)
  3. PAN
  4. Temporal arteritis
  5. Polymyalgia rheumatica
368
Q

FUO - Other causes:

A
  1. Granulomatous diseases (Sarco, Crohn).
  2. Drug fevers.
  3. Pulmonary embolism.
  4. Hemolytic anemia.
  5. Familial mediterranean fever (!).
  6. Gout.
  7. Subacute thyroiditis.
  8. Factitious illnesses.
369
Q

Approach to fever - Most sources define fever as:

A

Body temperature >37.5C measured by a modern ORAL thermometer.
–> Rectal thermometers are slightly higher than oral or axillary thermometer readings.

370
Q

Approach to fever - Hyperthermia vs fever:

A

Hyperthermia –> An elevation in body temperature not caused by “raising the thermostat” (ie, no change in the hypothalamic set-point).
–> Usually, caused by the inability of the body to dissipate heat.

371
Q

Approach to fever - Hyperthermia etiology:

A
  1. Neuroleptic malignant syndrome.
  2. Malignant hyperthermia
  3. Heat stroke.
372
Q

Approach to fever - Hyperthermia response to antipyretics:

A

Hyperthermia does NOT respond to antipyretics, but rather to external cooling measures (eg ice, fans) and mediacations specific to the cause (eg dantrolene for malignant hyperthermia).

373
Q

Approach to fever - Fever occurs when?

A

There is an elevation in the hypothalamic set-point. It is a natural response to an inflammatory process.
–> Usually responds to antipyretics.

374
Q

Approach to fever - Treat fever with antipyretics when:

A
  1. Fever is really hyperthermia.
  2. Fever is dangerously high: >41.
  3. Patient is pregnant.
  4. There is significant cardiopulmonary disease (incr. O2 demand may cause ischemia).
  5. The patient wants asymptomatic reliefs (chills, myalgias).
375
Q

Catheter-related sepsis - Etiology:

A
  1. Central venous catheters are a common cause of ever and sepsis in the hospital, especially in the ICU.
  2. MC organisms –> S.aureus and S.epi.
376
Q

Catheter-related sepsis - Risk factors:

A
  1. Emergent replacement of catheter.
  2. Femoral lines.
  3. Prolonged indwelling of the line.
377
Q

Catheter-related sepsis - How many patients with catheter-related sepsis have clinical evidence of infection at the site of insertion (ie erythema, purulence)?

A

ONLY 50% –> High index of suspicion is required.

378
Q

Catheter-related sepsis - If you suspect catheter-related, what should be done?

A

Promptly remove the catheter and send the tip for culture. This alone typically leads to resolution of fever and a decrease in leukocytosis.
–> Antibiotics are usually initiated. Narrow the spectrum once the organism is identified.

379
Q

Catheter-related sepsis - Only central venous catheter or also arterial or peripheral venous catheters are involved?

A

ONLY CENTRAL.

380
Q

Neutropenia - Definition:

A
  1. By absolute neutrophilic count (ANC) Severely increased risk of infection.
381
Q

Neutropenic fever - Etiology:

A
  1. Bone marrow failure (eg due to toxins, drugs).
  2. Bone marrow invasion.
  3. Peripheral causes (hypersplenism, SLE, AIDS).
  4. Isolated neutropenia (agranulocytosis) –> drug side effects.
382
Q

Neutropenic fever - Important to keep in mind:

A

Because neutropenia severely compromises the patient’s ability to mount an inflammatory response, fever may be the only manifestation of a raging infection.

383
Q

MC infections seen in neutropenic patients:

A
  1. Septicemia.
  2. Cellulitis.
  3. Pneumonia.
384
Q

Obtain the following for any neutropenic patient with a fever:

A
  1. CXR
  2. Panculture (blood, urine, sputum, line tips, wound) (!!!).
  3. CBC.
  4. Complete metabolic panel.
385
Q

Neutropenic fever management - If fever persists beyond 4-5days despite broad spectrum antibacterial therapy, then:

A

Give:

  1. Antifungal drugs - IV ampho B.
  2. Consider G-CSF.
386
Q

IM from EBV or CMV is milder?

A

From CMV.

387
Q

IM DDX in patients with fever, lymphadenopathy, and pharyngitis:

A
  1. Acute HIV infection.
  2. Strep infection.
  3. CMV.
  4. Toxoplasma.
388
Q

In which patients presenting with IM-like symptoms, is it important to perform diagnostic tests for HIV, CMV, and toxoplasma?

A

In pregnant patients –> Can have adverse effects on the fetus.

389
Q

One infection with EBV confers lifelong immunity?

A

YES - Usually it does.

390
Q

IM - incubation period:

A

2-5 weeks.

391
Q

IM - Signs:

A
  1. Lymphadenopathy - >90% of patients - Tonsillar or cervical (especially POSTERIOR cervical) –> May be quite enlarged, painful, and tender.
  2. Pharyngeal erythema and/or exudate - frequently present.
  3. Splenomegaly - Present in half of patients.
  4. Maculopapular rash.
  5. Hepatomegaly - In 10% of cases.
  6. Palatal petechiae and eyelid (periorbital) edema - may occur in a minority of cases.
392
Q

IM - Common lab abnormalities:

A
  1. Lymphocytosis.

2. Elevated aminotransferases.

393
Q

CMV mononucleosis - MC seen in:

A

Sexually active adolescents/young adults. Milder than EBV-associated IM.

394
Q

CMV mononucleosis - Features:

A
  1. Fevers
  2. Chills
  3. Fatigue
  4. Headaches
  5. Splenomegaly
395
Q

CMV mononucleosis - Cervical lymphadenopathy and pharyngitis?

A

It is usually, ABSENT.

396
Q

CMV mononucleosis - Heterophile antibodies?

A

Negative.

397
Q

IM - Diagnosis:

A
  1. Serology.
  2. Peripheral blood smear.
  3. Throat culture.
398
Q

IM - Serology:

A

A. Monospot test - detection of heterophile antibody.

  • -> Positive within 4 weeks of infection with EBV mono and are undetectable by 6 MONTHS.
  • -> NOT WITH CMV.
  • -> Rapid heterophile tests are highly sensitive and specific, particularly in adolescents.
399
Q

IM - Diagnosis - EBV-specific antibody testing:

A

Perform in cases in which diagnosis is not straightforward (usually done by indirect immunofluorescence microscopy or by ELISA).

400
Q

IM - Peripheral blood smear:

A

Usually reveals lymphocytic leukocytosis with large, atypical lymphocytes.

401
Q

IM diagnosis - Throat culture:

A

Perform if pharyngitis is present to RULE OUT a 2o infection with β-hemolytic strep.

402
Q

IM - Complications:

A
  1. Hepatitis.
  2. Neurologic complications (rare): meningoencephalitis, Guillain-Barre syndrome, Bell’s palsy.
  3. Splenic rupture - rare.
  4. Thrombocytopenia, hemolytic anemia.
  5. Upper airway obstruction due to lymphadenopathy - rare.
403
Q

IM - When to return to sports?

A

Concern is splenic rupture - Patients should wait 3 to 4 weeks from symptom onset before returning to sports as splenic rupture is very RARE after 4 weeks.

404
Q

Community-acquired pneumonia - Definition:

A

Occurs in the community OR within the first 72h of hospitalization.

Internal Medicine (107 decks)

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