Infectious Disease Flashcards

1
Q

Most commonly identified viruses
causing sporadic cases of acute encephalitis in immunocompetent adults

A

Herpesvirus, VZV, EBV

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2
Q

CSF sample to be taken for encephalitis

A

20mL, 5-10mL frozen for study

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3
Q

CSF profile of viral encephalitis

A

A. Lymphocytic pleocytosis,
*>5cells/mcL in immunocompetent indls
* Severely Immunocompromised: May fail to mount a CSF inflammatory response
* > 1000/mcL: Non-viral infection; arbovirus, mumps, LCMV
B. Mildly elevated protein conc
C. Normal gluc conc

  • Atypical Lymphocytes: CMV, HSV, enteroviruses
  • WNV encephalitis: Plasmacytoid or Mollaret-like large mononuclear cells
  • Persistent CSF neutrophilia: Bacterial infection, leptospirosis, amebic infection, and noninfectious processes - acute hemorrhagic leukoencephalitis
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4
Q

Primary diagnostic test for CNS infections caused by CMV, EBV, HHV-6, and enteroviruses

A

CSF PCR

  • HSV CSF PCR (sensitivity 96%; specificity ~99%)
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5
Q

CSF Ab testing of value to which patients

A

> 1 week in duration and CSF PCR negative for HSV

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6
Q

Diagnostic of WNV encephaltiis

A

WNV IgM Ab

  • IgM antibodies do not cross the blood-brain barrier, and their presence in CSF is therefore indicative of intrathecal synthesis.
  • Increases 10% per day after illness onset 70-80% by end of first week
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7
Q

Imaging findings of HSV encephalitis

A

Focal findings: consider HSV encephalitis
1. T2 weighted FLAIR or DW MRI: increased signal intensity in the frontotemporal, cingulate or insular regions of the brain
2. CT: focal areas of low absorption, mass effect, contrast enhancement
3. EEG: Periodic focal temporal lobe spikes on background of slow or low-amplitude (flattened act)
* periodic, stereotyped, sharp-and-slow complexes, one or both temporal lobes and repeating at regular intervals of 2-3 s

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8
Q

Imaging findings of WNV encephalitis

A

FLAIR: deep brain- thalamus, basal ganglia, brainstem abnormalities
EEG: Generalized slowing, anteriorly prominent

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9
Q

Imaging findings of VZV

A
  • multifocal areas of hemorrhagic and ischemic infarction, reflecting the tendency of this virus to produce a CNS vasculopathy rather than a true encephalitis
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10
Q

Imaging findings of CMV

A

Enlarged ventricles with areas of increased T2 on MRI- ventricles and subependymal enhancement on T1 weighted

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11
Q

Indication of Brain Biopsy for encephalitis (4)

A
  1. CSF PCR studies fail to lead to a specific diagnosis
  2. Have focal abnormalities on MRI
  3. No serologic evidence of autoimmune disease
  4. Show progressive clinical deterioration despite treatment with acyclovir and supportive therapy
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12
Q

Diagnosis of rabies virus antigen

A

Virus Ag in brain tissue or in neural innervation of hair follicles at the nape or neck

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13
Q

Treatment of HSV, EVB, VZV encephalitis

A

Acyclovir 10mg/kg IV every 8h (max 30mg/kg/d) x 21 days - started empirically if suspecting viral encephalitis, especially focal features

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14
Q

Treatment of HSV encephalitis

A

Ganciclovir
* Induction: 5mg/kg every 12h IV at constant rate over 1h (severe neurologic illness)
* Maintenance: 5mg/kg OD indefinitely
* Continued until: decline in CSF pleocytosis and reduced CSF CMV DNA copy number on quantitative PCR testing

Foscarnet
I: 60mg/kg every 8h constant infusion over 1h x 14-21 days
* Extend if failed to show a decline in CSF pleocytosis and reduction in CSF CMV DNA
M: 60-120mg/kg/d

Cidofovir: Nucleotide analogue for CMV retinitis
* 5mg/kg IV once weekly x 2 weeks then biweekly for 2 or more additional doses
* Prehydrated with normal saline 1L over 1-2h then probenecid
* Nephrotoxicity

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15
Q

MRI findings of progressive multifocal leukoencephalopathy

A
  • multifocal asymmetric, coalescing WM lesions located periventricularly in the centrum semiovale, in the parietal-occipital region and in cerebellum
    • Increased signal on T2 and FLAIR images
    • Decreased on T1-weighted images
    • HIV-PML: Non-enhancing
    • Immunomodulatory: Peripheral ring enhancement
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16
Q

Management of progressive multifocal leukoencephalopathy

A
  • 5HT2a receptor Mirtazapine: inhibit binding of JCV to its receptor on oligodendrocytes
  • Interferon alpha
  • Cytarabine: breakdown of BBB allows sufficient CSF penetration
  • Severe CNS inflammatory syndrome (IRIS): clinical worsening, CSF pleocytosis, appearance of new enhancing MRI lesions
    • Tx: IV glucocorticoids
  • Natalizumab: STOPPED
    • Tx: Plasma exchange or immunoadsorption
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17
Q

Initial presentation of Subacute Sclerosing Panencephalitis

A

Poor school performance, mood and personality changes

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18
Q

Most common organism for Community-acquired bacterial meningitis

A

Streptococcus pneumoniae (~50%)
Neisseria meningitidis (~25%)
Group B strep (~15%)
L. monocytogenes (~10%)

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19
Q

Most important predisposing condition for s. pneumoniae meningitis

A

pneumococcal pneumonia

  • RF: sinusitis or otitis media, alcoholism, DM, splenectomy, hypogammaglobulinemia, complement deficiency, head trauma with basilar skull fracture, CSF rhinorrhea
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20
Q

Bacteria that complicates neurosurgical procedures and head trauma associated CSF rhinorrhea or otorrhea

A

Gram negative bacilli

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21
Q

Bacteria following invasive neurosurgical procedures such as shunting, ommaya reservoirs

A

S. aureus and CONS

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22
Q

Presentation of patient’s with raised ICP

A
  • Deteriorating or reduced level of consciousness, papilledema, dilated poorly reactive pupils, 6th nerve palsies, decerebrate posturing, cushing reflex
    • Cushing reflex: bradycardia, hypertension, irregular respirations
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23
Q

Most disastrous complication of increased ICP

A

Cerebral herniation

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24
Q

Indications to proceed with lumbar puncture without prior neuroimaging (4)

A
  1. Immunocompetent patient
  2. no known history of recent head trauma
  3. a normal level of consciousness
  4. no evidence of papilledema or focal neurologic deficits
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25
Q

CLASSIC CSF Abnormalities in BACTERIAL MENINGITIS

A
  1. PMN leukocytosis (>100 cells/uL in 90%)
  2. Decreased CSF Glucose
    • <40 mg/dL
    • CSF/serum glucose ratio of <0.4 in ~60%
  3. Increase protein concentration (>45 mg/dL in 90%)
  4. Increased opening pressure (>180 mmH2O in 90%)
    * CSF Glucose concentrations <40mg/dl (Abnormal)
    * CSF glucose concentration of zero= bacterial meningitis
    * CSF/serum glucose <0.6 = CSF glucose con’c is LOW
    * CSF/serum glucose <0.4 = HIGHLY suggestive of BAC MEN (may be seen in fungal, TB and carcinomatous meningitis)
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26
Q

Empirical therapy of Community-Acquired Suspected bacterial meningitis in children and adults

A

Dexamethasone + Third- or Fourth-Gen cephalosporins (Ceftriaxone/Cefotaxime/Cefepime) and Vancomycin plus (Acyclocivr or Doxycycline)

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27
Q

Treatment for susceptible S. pneumonia, group B strep, H. influenza and adequate coverage for N. meningitides

A

Ceftriaxone or Cefotaxime

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28
Q

When to add Ampicillin to empirical regimen in Bac Men?

A

For coverage of L. monocytogenes, <3 months of age, those > 55, those with imapired cell mediated immunity

  • AMPICILLIN for at least 3 weeks
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29
Q

When to add Metronidazole to empirical regimen in Bac Men?

A

Gram-negative anaerobes in patients with otitis, sinusitis,
or mastoiditis

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30
Q

Empiric regimen for HA meningitis, particulalry during neurosurgical procedures

A
  • Cover for Staph, gram neg including P. aeruginosa
  • Vancomycin and Ceftazidime OR Meropenem
  • MEROPENEM SHOULD NOT BE USED AS MONOTHERAPY!!!
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31
Q

Treatment of Meningococcal Meningitis?

A
  • PENICILLIN G - antibiotic of choice for Penicillin-seinsitive
  • CEFOTAXIME / CEFTRIAXONE - if with Penicillin resistance
  • Uncomplicated: 7 day course
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32
Q

Meningococcal hemoprophylaxis for index case and close all contacts (3)

A
  1. RIFAMPIN 600 mg every 12 h for 2 days in adults
  2. Alternative: Azithromycin 500 mg x1 dose
  3. Alternative: Ceftriaxone 250 mg IM x1dose
  • Close contacts are defined as individuals who have had contact with oropharyngeal secretions, either through kissing or by sharing toys, beverages, or cigarettes.
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33
Q

When do you repeat LP in patients with S. pneumoniae meningitis?

A

Repeat LP performed 24-36H after initiation of antimicrobial therapy to document sterilization of CSF

Failure to sterilize the CSF after 24–36 h of antibiotic therapy should be considered presumptive evidence of antibiotic resistance.

Penicillin- and cephalosporin-resistant strains of S. pneumoniae who do not respond to intravenous vancomycin alone may benefit from the addition of intraventricular vancomycin.

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34
Q

Regimen to be added with Listeria Menigitides for critically ill patient

A

Gentamicin (2 mg/kg loading dose, then 7.5 mg/kg per day
given every 8 h and adjusted for serum levels and renal function).

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35
Q

Alternative for patients with L. monocytogenes menigitis with penicillin-allergy?

A
  • COTRIMOXAZOLE - alternative in penicillin-allergic patients
    • TMP 10-20mg/kg/day
    • SMX 50-100mg/kg/d every 6 hours
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36
Q

Regimen for susceptible strains of S. aureus or CONS

A

NAFCILLIN

37
Q

Drug of choice for MRSA and for patients allergic to penicillin

A

VANCOMYCIN

  • If the CSF is not sterilized after 48 h of intravenous vancomycin therapy, then either intraventricular or intrathecal vancomycin, 20 mg once daily, can be added.
38
Q

Regimen for gram negative bacilliary meningitis (susceptible and with P. aeruginosa), and recommended duration?

A

cefotaxime, ceftriaxone, and ceftazidime—are equally
efficacious for the treatment of gram-negative bacillary meningitis
If with P. aeroginosa: Ceftazidime or Meropenem
Recommended duration: 3 weeks

39
Q

When to give adjuvant Dexamethasone in Meningitis?

A
  • 20 mins BEFORE antibiotics, or not later than concurrent with the first dose of antibiotics - inhibits the production of TNF-alpha abs macrophages and micoglia only if it is administered before the cells are activated by endotoxin
40
Q

Emergency treatment of increased ICP (3)

A
  • Elevation of patient’s head to 30-45 degrees
  • Intubation and hyperventilation (PaCO2 25-30mmHg)
  • Mannitol
41
Q

The risk of death from bacterial meningitis increases with (6)

A
  1. Decreased level of sensorium on admission
  2. Onset of seizures within 24H of admission
  3. Signs of increased ICP
  4. Infants and elderly >50
  5. Presence of co-morbidities including SHOCK and/or need for MECH VENT
  6. Delay initiation of treatment
42
Q

CSF findings of viral meningitis

A
  1. Pleocytosis (25–500/μL, can exceed 1,000/μL in some infections like LCMV or mumps).
    * WNV: PMN pleocytosis in 45%, persist for week or longer before shifting to lymphocytic pleocyotosis
    * CMV: PMN pleocytosis with low glucose
  2. Normal or slightly elevated protein concentration: 0.2–0.8 g/L (20-80mg/dL)
    • Normal glucose concentration
      • May be low in 10–30% of cases (e.g., mumps, LCMV).
  3. Normal or mildly elevated opening pressure: 100–350 mmH2O
43
Q

Gold standard diagnostic procedure for viral meningitis

A

Polymerase Chain Reaction (PCR)
* Enterovirus, HSV, VZV, CMV, EBV, and HHV-6
* HSV DNA in recurrent episodes of aseptic meningitis, even with negative viral cultures.

44
Q

Clues for Bacterial Meningitis vs. Aseptic Meningitis

A
  • CSF protein >0.5 g/L: Sensitivity 89%, specificity 78%.
  • Serum procalcitonin >0.5 ng/mL: Sensitivity 89%, specificity 89%.
  • Bacterial meningitis score (negative predictive value 99.7%):
    • Negative CSF Gram’s stain.
    • CSF neutrophil count <1000 cells/μL.
    • CSF protein <80 mg/dL.
    • Peripheral ANC <10,000 cells/μL.
    • No prior history/current presence of seizures.
45
Q

When to hospitalize patients with viral meningitis?

A
  1. immunocompromised patients
  2. altered consciousness, seizures
  3. Atypical CSF profiles
  4. focal neurological signs and symptoms suggesting possibility of encephalitis or parenchymal brain involvement
46
Q

Management of HSV-1, HSV-2, EBV, VZV meningitis

A

IV acyclovir (15–30 mg/kg/day in 3 doses) followed by oral drugs (acyclovir, famciclovir, valacyclovir)
Total course: 7–14 days.

47
Q

Lab findings of tuberculous meningitis?

A

CSF Findings:
1. Elevated opening pressure
2. ymphocytic pleocytosis (10-500
3. elevated protein 1-5g/L
4. decreased glucose 20-40mg/dL.
Smear: AFB in the CSF (often 10–40% positive).
Culture: Takes 4-8 weeks; Positive in ~50% of cases, gold standard.
PCR: For M. tuberculosis DNA.

48
Q

S/Sx, lab findings highly suggestive of tuberculous meningitis

A

Unrelenting headache, Stiff neck, fatigue, night sweats, and fever with a CSF lymphocytic pleocytosis
and a mildly decreased glucose concentration

49
Q

Management of tuberculous meningitis

A
  • Empirical therapy: Start with isoniazid (300 mg/d), rifampin (10 mg/kg/d), pyrazinamide (30 mg/kg/d), ethambutol (15–25 mg/kg/d), and pyridoxine (50 mg/d).
  • Adjustments: Discontinue ethambutol if M. tuberculosis is sensitive; stop pyrazinamide after 8 weeks if responsive.
  • Duration: Isoniazid and rifampin for 6–12 months, extended to 9–12 months for slow resolution or with positive mycobacterial cultures of CSF.
  • Adjunct therapy: Dexamethasone (12–16 mg/d tapered over 6 weeks) for HIV-negative patients.
50
Q

Historical clue of C. meomorfans, H. capsulatum, C. immitis

A
  • MC: C. neoformans - soil and bird excreta
    • H. capsulatum: Ohio and Mississippi River valleys of central US and central and south america
    • C. immitis: Desert areas
51
Q

Most important pathogen of brain abscess for immunocompotent host

A
  • Streptococcus spp (anaerobic, aerobic and viridans 40%)
    • Enterobacteriaceae (Proteus spp, E coli, KPN 25%)
    • Anaerobes (Bacteroides spp, Fusobacterium spp 30%)
    • Staphylococci - 10%
  • IMMUNOCOMPROMISED HOST
    • HIV, Transplant patient, Cancer, Immunosuppressed
    • Nocardia, Toxoplasma gondii, Candida and C. neoformans
52
Q

What stage of brain abscess presents with perivascular infiltration of inflammatory cells, surrounds a central core of coagulative necrosis and marked edema?

A

Early Cerebritis
Presents within day 1-3

53
Q

What stage of brain abscess presents with pus formation –> enlargement of the necrotic center, surrounded by inflammatory infiltrate of macrophages and fibroblast?

A

Late cerebritis (D 4-9)
More distinct edema
thin capsule of fibroblasts and reticular fibers gradually develops, and the surrounding area of cerebral edema becomes more distinct

54
Q

What stage of brain abscess presents with formation of a capsule and shows ring enlargement of MRI?

A

Early capsule formation (D 10-13)

55
Q

What stage of brain abscess presents well-formed necrotic center surrounded by a dense collagenous capsule?

A

Late capsule formation (Day 14 and beyond)
* Marked glosis –> may contribute to seizure

56
Q

Classic triad of brain abscess?

A

Headache, Fever, Focal Neurologic deficit
* Hemiparesis (frontal)
* Aphasia (dysphasia) or visual field defects (upper homonymous quandrantinopia (Temporal)
* Nystagmus and ataxia: Cerebellar
* Increased ICP: Cerebellum

57
Q

Optimal therapy of brain abscesses?

A

High Dose Parenteral antibiotics + Neurosurgical drainage

IMMUNOCOMPETENT COMMUNITY ACQUIRED
Third- or fourth- generation cephalosporin and Metronidazole
For PENETRATING HEAD TRAUMA / RECENT NEUROSURGICAL PROCEDURE
* Ceftazidime / Meropenem for P. aeruginosa
* PLUS Vancomycin for staph

58
Q

Indication of doing craniotomy or craniectomy in patient with brian abscess (2)?

A

Multiloculated abscesses
Unsuccessful stereotactic aspiration

59
Q

Indication of medical therapy only on patients with brain abscess (4) and how long should parenteral antibiotic therapy given?

A
  1. For neurologically inaccessible
  2. Small <2-3cm or Nonencapsulated abscesses- cerebritis
  3. Too tenuous to allow performance of a neurosurgical procedure

Minimum of 6-8 weeks of parenteral antibiotic therapy

60
Q

How long should prophylactic anticonvulsant therapy be given to patients with brain abscess?

A

Continued for 3 months after resolution of abscess - withdrawal based on EEG
* NORMAL- slowly withdrawn
* Repeat EEG after medications were discontinued

61
Q

Indication of glucocorticoid therapy (Dexamethasone 10mg IV every 6 hours) in brain abscess (3)?

A

Substantial periabscess edema
Mass effect
Increased ICP

62
Q

How to document resolution of brain abscess?

A

SERIAL MRI/CT SCANS -
* once or twice monthly
* If antibiotic therapy alone: More frequent studies

63
Q

What is the most common manifestation of neurocysticercosis?

A

New-onset partial seizures with/without secondary generalization

64
Q

Stages of neurocysticerrcosis based on MRI/CT findings?

A
  1. Vesicular Stage:
    • Cystic lesions with scolex visible within cyst
    • No significant surrounding edema.
  2. Colloidal Stage:
    • Peripheral enhancement with post-contrast imaging
    • Substantial surrounding edema on T2 images.
  3. Granulonodular Stage:
    • Homogenous enhancement on postcontrast imaging.
    • No surrounding edema on FLAIR images.
  4. Nodular Calcified-Stage:
    • Parenchymal brain calcifications, most common finding and evidence that the parasite is no longer viable - Best detected on CT; small calcifications detected by SWI on MRI.
65
Q

Mmost common finding and evidence that the parasite is no longer viable on imaging

A

Parenchymal brain calcifications
Nodular-Calcified stage

66
Q

Recommended test for all patients suspected with neurocysticercosis?

A

Funduscopic exam

67
Q

Most common source of liver abscess infection?

A

Disease of the biliary tract: MC source
Common isolates: Enteric gram-negative aerobic bacilli and enterococci

  • Hematogenous or contiguous sites of infection: S. aureus or a streptococcal species- Streptococcus milleri group
68
Q

Single most reliable lab findings of liver abscess

A

Elevated serum alkaline phosphatase

  • Elevated serum alkaline phosphatase: single most reliable lab findings
  • Bilirubin (50%), aminotransferase - AST (48%)

Imaging:
CXR
New elevation of right hemidiaphragm
Right basilar infiltrate
Right pleural effusion

69
Q

Surgical indication for percutaneous drainage of liver abscess (6)

A
  • (+) multiple, sizable abscesses
    * Viscous abscess- plug the catheter
    * Associated disease requiring surgery
    * (+) yeast
    * Communication with an untreated obstrcructed biliary tree
    * Lack of clinical response to percutaneous drainage in 4-7 days
70
Q

Treatment of candidal liver abscess

A
  • Liposomal amphotericin B (3–5 mg/kg IV daily) or an echinocandin, with subsequent fluconazole therapy
  • Fluconazole alone (6 mg/kg daily) may be used (Stable, susceptible organism)
71
Q

What organisms require echocardiogram when cultures on blood?

A
  1. S. sanguinis
  2. S. gallolyticus
  3. S. mutans
72
Q

What is the organism most frequently isolated in splenic abscesses?

A

Streptoccus spp. (Most)
Followed by s. aureus

(Endocarditis)

73
Q

Vaccination prior to splenectomy

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Neisseria meningitidis
74
Q

What is the treatment of choice for epididymitis caused by N. gonorrhoeae or C. trachomatis?

A

Ceftriaxone 500mg IM as a single dose followed by Doxycycline 100mg orally 2x a day for 10 days

75
Q

Antifungal drug resistance is one of the hallmarks of infection with this organism

A

C. auris

Elevated minimal inhibitory concentrations (MICs) to all three major antifungal classes—azoles, echinocandins, and polyenes—resulting in limited treatment options

76
Q

Factors that influence mortality risk of PCP (6)

A
  1. Patient’s age
  2. Degree of immunosuppression
  3. Presence of preexisting lung disease
  4. Low serum albumin level
  5. Need for mechanical ventilation
  6. Development of a pneumothorax.
77
Q

The induction of vascular permeability and shock in dengue is increased with (6)

A
  1. Presence or absence of enhancing and non-neutralizing antibodies
  2. Age < 12
  3. Female
  4. White > Black
  5. Nutritional status
  6. Timing and sequence of infections
    * Dangerous: Dengue virus 1 infection followed by dengue virus 2 infection vs dengue virus 4 infection followed by dengue virus 2 infection
78
Q

Central to the pathogenesis of falciparum malaria (3)

A
  1. Rosette: Infected RBCs adhere to uninfected RBC
  2. Agglutination: Infected RBCs also adhere to infected RBCs
  3. Cytoadherence

cytoadherence, rosetting, and agglutination

79
Q

Best biochemical prognosticators in severe malaria?

A

Plasma concentrations of bicarbonate or lactate

80
Q

Laboratory test generally accepted as the best indicator of the immediate state of immunologic competence of the patient with HIV infection

A

CD4+ T cell count

81
Q

Preferred antibiotic therapy for patients with tetanus?

A

Metronidazole (400 mg rectally or 500 mg IV every 6 h for 7 days) is preferred for antibiotic therapy.

82
Q

Hallmark feature of enteric fever

A

Variable fever and abdominal pain

83
Q

What vaccines are not recommended if with history of allergic reaction to latex (2)

A
  1. Serogroup B meningococcal
  2. Hepatitis A
84
Q

What vaccines are not recommended if with history of allergic reaction to gelatin or neomycin (3)

A
  1. MMR
  2. Varicella
  3. Zoster
85
Q

What vaccines are not recommended if with history of allergic reaction to yeast (2)?

A
  1. HPV
  2. Hepaitis B
86
Q

Which trematode is associated with crayfish or crabs?

A

Paragonimus westermani

  • Half-cooked fish: Chlonochis sinensis
87
Q

What is the drug of choice for fascioliasis?

A

Triclabendazole

88
Q
A