Infectious Diseases Flashcards
(105 cards)
1
Q
What tetanus prophylaxis is indicated for a clean/minor wound in a patient with ≥3 tetanus toxoid doses, and last dose <10 years ago?
A
No tetanus vaccine or TIG needed.
2
Q
What tetanus prophylaxis is indicated for a clean/minor wound in a patient with ≥3 tetanus toxoid doses, and last dose ≥10 years ago?
A
Tetanus toxoid–containing vaccine; no TIG.
3
Q
What tetanus prophylaxis is indicated for a dirty/severe wound in a patient with ≥3 tetanus toxoid doses, and last dose <5 years ago?
A
No tetanus vaccine or TIG needed.
4
Q
What tetanus prophylaxis is indicated for a dirty/severe wound in a patient with ≥3 tetanus toxoid doses, and last dose ≥5 years ago?
A
Tetanus toxoid–containing vaccine; no TIG.
5
Q
What tetanus prophylaxis is indicated for a clean/minor wound in a patient who is unimmunized, uncertain, or has <3 tetanus toxoid doses?
A
Tetanus toxoid–containing vaccine only; no TIG.
6
Q
What tetanus prophylaxis is indicated for a dirty/severe wound in a patient who is unimmunized, uncertain, or has <3 tetanus toxoid doses?
A
Tetanus toxoid–containing vaccine plus tetanus immune globulin (TIG).
7
Q
When is tetanus immune globulin (TIG) indicated in tetanus prophylaxis?
A
For dirty/severe wounds in patients with <3 tetanus toxoid doses or uncertain vaccination status.
8
Q
What defines a ‘dirty/severe’ wound requiring tetanus prophylaxis?
A
Wounds with contamination (e.g., dirt, bite, plant matter) or deep/puncture wounds.
9
Q
How many tetanus toxoid doses are considered adequate immunization for determining need for TIG?
A
3 or more tetanus toxoid–containing doses.
10
Q
For a child with a contaminated wound who received 4 DTaP doses, including one at age 4, and last dose <5 years ago—what is the appropriate tetanus prophylaxis?
A
None needed; adequately immunized with recent dose.
11
Q
What defines asymptomatic bacteriuria during pregnancy?
A
Positive urine culture (≥100,000 colonies/mL) in an asymptomatic patient.
12
Q
When should pregnant women be screened for asymptomatic bacteriuria?
A
At the initial prenatal visit.
13
Q
Why is treatment of asymptomatic bacteriuria during pregnancy important?
A
To prevent progression to UTI and complications like preterm birth.
14
Q
What are first-line antibiotics for treating asymptomatic bacteriuria during pregnancy?
A
- Cefpodoxime
- Amoxicillin-clavulanate
- Fosfomycin
15
Q
How is acute cystitis defined in pregnancy?
A
A symptomatic patient with a positive urine culture.
16
Q
What are common symptoms of acute cystitis in pregnancy?
A
- Dysuria
- Urinary frequency/urgency
- Positive leukocyte esterase on urinalysis
17
Q
What is the most common pathogen causing acute cystitis in pregnancy?
A
Escherichia coli.
18
Q
Name two less common pathogens for acute cystitis in pregnancy.
A
- Proteus mirabilis
- Klebsiella pneumoniae
19
Q
What are the first-line antibiotics for acute cystitis in pregnancy?
A
- Cefpodoxime
- Amoxicillin-clavulanate
- Fosfomycin
20
Q
Why are nitrofurantoin and TMP-SMX generally avoided in late pregnancy?
A
Risk of neonatal hemolysis (nitrofurantoin) and kernicterus (TMP-SMX).
21
Q
When can nitrofurantoin and TMP-SMX be safely used during pregnancy?
A
In the second trimester.
22
Q
Why is TMP-SMX avoided in the first trimester of pregnancy?
A
Risk of neural tube defects due to folate antagonism.
23
Q
Why are fluoroquinolones contraindicated in pregnancy?
A
They are toxic to fetal cartilage development.
24
Q
Why are tetracyclines avoided in pregnancy?
A
They impair fetal long-bone development and stain deciduous teeth.
25
Why is clindamycin not used to treat acute cystitis?
It lacks coverage for gram-negative bacteria.
26
After completing antibiotic treatment for bacteriuria in pregnancy, what is done next?
Repeat urine culture 1 week after treatment to confirm cure.
27
What are the classic presenting symptoms of acute pyelonephritis in pregnancy?
Fever, nausea, flank pain, and costovertebral angle tenderness
28
What are the key risk factors for developing pyelonephritis during pregnancy?
Asymptomatic bacteriuria, diabetes mellitus, age <20, nulliparity, pregestational diabetes, sickle cell disease/trait, and tobacco use
29
What are the most common pathogens causing pyelonephritis in pregnancy?
Escherichia coli, Klebsiella, Enterobacter, and Group B Streptococcus
30
What are the major complications of pyelonephritis in pregnancy?
Preterm labor, low birth weight, acute respiratory distress syndrome, pulmonary edema, renal abscess, papillary necrosis, and renal failure
31
What is the recommended initial management for pyelonephritis in pregnancy?
Hospitalization for intravenous hydration and empiric treatment with broad-spectrum beta-lactam antibiotics (e.g., ceftriaxone, cefepime)
32
Why are nitrofurantoin and trimethoprim-sulfamethoxazole not used to treat pyelonephritis in pregnancy?
Nitrofurantoin does not achieve adequate renal levels; trimethoprim-sulfamethoxazole is associated with birth defects in the first trimester and neonatal kernicterus in the third trimester
33
Why are fluoroquinolones avoided in pregnant patients with pyelonephritis?
Fluoroquinolones are toxic to fetal cartilage development
34
When is renal ultrasound indicated in pregnant patients with pyelonephritis?
If the patient remains febrile after 48–72 hours of broad-spectrum antibiotics, to evaluate for complications such as renal abscess
35
What is the duration of oral antibiotic therapy after initial IV treatment for pyelonephritis in pregnancy?
10–14 days
36
What is the role of daily suppressive therapy after treating pyelonephritis in pregnancy?
It is initiated and maintained until 6 weeks postpartum to prevent recurrence
37
Why is outpatient management of pyelonephritis not recommended during pregnancy?
Due to the high risk of complications such as pulmonary edema and the need for close monitoring and IV antibiotics
38
What physiologic changes in pregnancy can complicate the diagnosis of pyelonephritis?
Dilation of the ureters and renal pelvis due to elevated progesterone and the expanding uterus
39
What is the peak incidence age range for acute rheumatic fever (ARF)?
5–15 years old.
40
Which gender is more commonly affected by acute rheumatic fever?
Girls (twice as common as boys).
41
What is the most important risk factor for developing acute rheumatic fever?
Untreated group A streptococcal pharyngitis.
42
What are the major Jones criteria for diagnosing acute rheumatic fever?
Migratory arthritis, carditis, subcutaneous nodules, erythema marginatum, Sydenham chorea.
43
What are the minor Jones criteria for diagnosing acute rheumatic fever?
Fever, arthralgia, elevated ESR and/or CRP, prolonged PR interval on ECG.
44
How is the diagnosis of acute rheumatic fever confirmed using the Jones criteria?
By the presence of 2 major criteria or 1 major and 2 minor criteria.
45
What is Sydenham chorea and how does it present in acute rheumatic fever?
It is a major Jones criterion, presenting as emotional lability, decline in school performance, and distal hand movements progressing to facial grimacing and foot jerking; movements are irregular and rapid.
46
When does Sydenham chorea typically develop after a streptococcal infection?
1–8 months after the initial infection.
47
What late sequela is most associated with acute rheumatic fever?
Valvular disease, particularly mitral stenosis.
48
What is the recommended prevention for acute rheumatic fever?
Penicillin for group A streptococcal pharyngitis.
49
What cardiac complication should be evaluated in a patient with murmur and suspected ARF?
Carditis, which should be evaluated by echocardiography.
50
What are the earliest neurologic manifestations of Sydenham chorea in children?
Emotional lability and decline in school performance.
51
What physical exam findings are seen in Sydenham chorea?
Distal hand movements, facial grimacing, foot jerking, decreased strength, delayed patellar reflex relaxation, and pronator drift.
52
What is the hallmark rash of early localized Lyme disease and how does it present?
Erythema migrans, a slowly spreading, erythematous rash that starts as a confluent macule and develops into a bull’s-eye shape with central clearing.
53
What are the common symptoms of early localized Lyme disease?
Erythema migrans, fatigue, headache, myalgia, and arthralgia.
54
How is early localized Lyme disease diagnosed?
Clinically, based on symptoms and exposure history, because serologic testing is often falsely negative in early infection.
55
What is the first-line treatment for early localized Lyme disease?
Oral doxycycline.
56
What are the clinical features of early disseminated Lyme disease?
Multiple erythema migrans, unilateral or bilateral cranial nerve palsy (especially CN VII), meningitis, carditis (e.g., AV block), and migratory arthralgia.
57
What is the recommended diagnostic approach for early disseminated or late Lyme disease?
Serologic testing with B. burgdorferi enzyme-linked immunosorbent assay (ELISA) followed by Western blot.
58
What are the severe manifestations of Lyme disease that require intravenous therapy?
Carditis with advanced atrioventricular block, radiculopathy, and meningitis.
59
What is the preferred intravenous antibiotic for severe Lyme disease manifestations?
Intravenous ceftriaxone.
60
What are the clinical features of late Lyme disease?
Arthritis, encephalitis, and peripheral neuropathy.
61
Why is serologic testing not recommended for early localized Lyme disease?
Because the humoral antibody response is not fully developed, leading to frequent false negatives.
62
What is the typical time frame for the development of early localized Lyme disease symptoms after a tick bite?
Within 1–2 weeks.
63
What is the prognosis for early localized Lyme disease with appropriate treatment?
Treatment with oral doxycycline is generally curative.
64
What is the hallmark rash of early localized Lyme disease and how does it present?
Erythema migrans, a slowly spreading, erythematous rash that starts as a confluent macule and develops into a bull’s-eye shape with central clearing.
65
What are the common symptoms of early localized Lyme disease?
Erythema migrans, fatigue, headache, myalgia, and arthralgia.
66
How is early localized Lyme disease diagnosed?
Clinically, based on symptoms and exposure history, because serologic testing is often falsely negative in early infection.
67
What is the first-line treatment for early localized Lyme disease?
Oral doxycycline.
68
What are the clinical features of early disseminated Lyme disease?
Multiple erythema migrans, unilateral or bilateral cranial nerve palsy (especially CN VII), meningitis, carditis (e.g., AV block), and migratory arthralgia.
69
What is the recommended diagnostic approach for early disseminated or late Lyme disease?
Serologic testing with B. burgdorferi enzyme-linked immunosorbent assay (ELISA) followed by Western blot.
70
What are the severe manifestations of Lyme disease that require intravenous therapy?
Carditis with advanced atrioventricular block, radiculopathy, and meningitis.
71
What is the preferred intravenous antibiotic for severe Lyme disease manifestations?
Intravenous ceftriaxone.
72
What are the clinical features of late Lyme disease?
Arthritis, encephalitis, and peripheral neuropathy.
73
Why is serologic testing not recommended for early localized Lyme disease?
Because the humoral antibody response is not fully developed, leading to frequent false negatives.
74
What is the typical time frame for the development of early localized Lyme disease symptoms after a tick bite?
Within 1–2 weeks.
75
What is the prognosis for early localized Lyme disease with appropriate treatment?
Treatment with oral doxycycline is generally curative.
76
What are the typical clinical features of 'walking pneumonia' caused by Mycoplasma pneumoniae?
Low-grade fever, sore throat, persistent cough, and chest x-ray showing bilateral patchy infiltrate.
77
Why can’t Mycoplasma pneumoniae be treated with beta-lactam antibiotics?
Mycoplasma lacks a cell wall, so beta-lactam antibiotics (which target peptidoglycan) are ineffective.
78
Which antibiotics are effective for treating Mycoplasma pneumoniae?
Bacterial protein synthesis inhibitors such as macrolides or tetracyclines.
79
Why does Mycoplasma pneumoniae not show up on Gram stain?
It completely lacks a cell wall, so it cannot retain Gram stain.
80
What is the role of trimethoprim-sulfamethoxazole in pneumonia treatment?
It is first-line therapy for Pneumocystis pneumonia, not for Mycoplasma or Chlamydia pneumoniae.
81
What are the typical radiographic findings in Mycoplasma pneumoniae infection?
Bilateral patchy interstitial infiltrates on chest x-ray.
82
Which pathogens are common causes of atypical pneumonia besides Mycoplasma?
Chlamydia pneumoniae and Legionella pneumophila.
83
What distinguishes Legionella pneumonia from Mycoplasma pneumoniae clinically?
Legionella is associated with gastrointestinal symptoms, higher fever, and more severe illness with lobar infiltrate.
84
What is the educational objective regarding Mycoplasma pneumoniae and antibiotic choice?
Mycoplasma pneumoniae is a leading cause of atypical pneumonia and must be treated with protein synthesis inhibitors, not beta-lactam antibiotics, due to its lack of a cell wall.
85
What is the most likely cause of fever in a patient with a tunneled hemodialysis catheter and no localizing symptoms?
Catheter-related bloodstream infection (CRBSI)
## Footnote
CRBSI is a common complication in patients with hemodialysis catheters.
86
What are the most common pathogens causing CRBSI in hemodialysis patients?
* Coagulase-negative staphylococci
* Staphylococcus aureus
* Gram-negative bacilli
## Footnote
These pathogens are frequently isolated in CRBSI cases among hemodialysis patients.
87
What is the initial workup for suspected catheter-related bloodstream infection?
Obtain 2 sets of blood cultures (one from a peripheral site and one from the catheter) and start empiric antibiotics
## Footnote
This approach helps confirm the diagnosis and initiate appropriate treatment.
88
What empiric antibiotics are recommended for suspected CRBSI in hemodialysis patients?
* Vancomycin
* Cefepime (or gentamicin)
## Footnote
These antibiotics cover a broad range of potential pathogens associated with CRBSI.
89
What are the indications for immediate catheter removal in CRBSI?
* Severe sepsis
* Hemodynamic instability
* Evidence of metastatic infection (e.g., endocarditis)
* Pus at the catheter exit site
* Continued symptoms after 72 hours of empiric antibiotics
## Footnote
Immediate removal is critical in these situations to prevent further complications.
90
When should a long-term hemodialysis catheter be removed in CRBSI?
If blood cultures grow Staphylococcus aureus, Pseudomonas aeruginosa, or fungi (e.g., Candida)
## Footnote
These organisms are associated with higher risks of complications and warrant catheter removal.
91
What should be done if a catheter is not immediately removed in a stable patient with CRBSI?
* Catheter change over a guidewire (once afebrile and stable)
* Antibiotic lock therapy after each dialysis session
## Footnote
These measures help manage the infection while minimizing risks associated with catheter retention.
92
When is empiric caspofungin indicated in CRBSI?
For patients with risk factors such as total parenteral nutrition, prolonged broad-spectrum antibiotics, hematologic malignancy, solid organ transplant, femoral catheterization, or Candida colonization at multiple sites
## Footnote
These factors increase the likelihood of fungal infections, necessitating antifungal coverage.
93
Do most hemodialysis patients with CRBSI require empiric antifungal coverage?
No, empiric caspofungin is not typically required unless specific risk factors are present
## Footnote
The routine use of antifungals is reserved for higher-risk patients.
94
What is the educational objective regarding CRBSI management in hemodialysis patients?
Initiate empiric vancomycin plus cefepime (or gentamicin); remove the catheter only for severe sepsis, hemodynamic instability, pus, metastatic infection, or persistent symptoms after 72 hours of antibiotics
## Footnote
This objective emphasizes the importance of timely and appropriate management of CRBSI.
95
What percentage of patients with Staphylococcus aureus bacteremia develop metastatic infection?
Up to 40%.
96
Which sites are most commonly affected by metastatic infection in Staphylococcus aureus bacteremia?
Heart valves, lungs, and osteoarticular structures (such as the spine).
97
What clinical findings should raise suspicion for vertebral osteomyelitis in a patient with Staphylococcus aureus bacteremia?
Persistent fever, continued leukocytosis, and worsening back or neck pain that localizes to the affected disc space.
98
How sensitive are blood cultures for detecting vertebral osteomyelitis in Staphylococcus aureus bacteremia?
Blood cultures are positive in only about 50% of cases.
99
What is the diagnostic test of choice for suspected vertebral osteomyelitis?
MRI of the spine.
100
Why are plain radiographs not reliable in early vertebral osteomyelitis?
They are often normal during the first two weeks of infection and cannot rule out early osteomyelitis.
101
After MRI suggests vertebral osteomyelitis, what is required for confirmation?
Open or CT-guided biopsy.
102
What is the typical treatment duration for Staphylococcus aureus vertebral osteomyelitis?
Prolonged vancomycin therapy, often for months.
103
When should MRI of the spine be prioritized over altering antibiotics in Staphylococcus aureus bacteremia with back pain?
When there is persistent fever, leukocytosis, and focal back pain despite initial antibiotic therapy.
104
Why are tagged white blood cell scans rarely used for diagnosing osteomyelitis?
Findings are generally nonspecific.
105
What is the educational objective regarding Staphylococcus aureus bacteremia and focal symptoms?
Always suspect metastatic infection (such as vertebral osteomyelitis) in patients with persistent fever, leukocytosis, and new focal symptoms; diagnosis is generally made by spinal MRI and confirmed with biopsy.
