Infectious Diseases Case Conference

1
Infectious Diseases Case Conference
Pimpawan Boapimp, MD Wake Forest Baptist Medical
Center November 29, 2004
2
HPI

• 32 Y/O hispanic male with no significant PMH
• 2 weeks of headache, fever, and eye pain.
• Was seen by ophthalmologist and diagnosed with
  toxoplasmosis chorioretinitis
• (from eye exam and high toxoplasmosis titer)
• Was started on pyrimethamine and sulfadiazine at
  that time.

3
HPI

• Came to ED 2 days PTA with HA, fever
• VS T 97.2 P 112, RR 20 BP 166/90
• CT brain without contrast showed no abnormality.
• Symptoms relieved with migraine cocktail
  Compazine 10 mg, Benadryl 26 mg, Decadron 10 mg
  IV and was D/Cd home

4
HPI

• Symptoms returned so he came to ED again
• VS T 100.8, P 110, RR 20, BP 142/76
• CT brain with contrast- WNL
• LP was done.
• Pt was admitted to Internal Medicine service.

5

• Meds
• Leucovorin 5 milligrams p.o. QD
• Sulfadiazine 1,000 milligrams p.o QID
• Pyrimethamine 25 milligrams p.o. QD

6
Physical Examination

• VS T 100.8 P 110 RR 20 BP 140/76 PO-
  RA
• GA AO X 3, febrile, NAD
• HEENT PERRLA, EOMI
• CHEST CTA bilaterally.
• HEART RSR, nl S1,S2.
• ABD Benign.
• EXT No edema.
• SKIN Generalized maculopapular rash.

7
Diagnostic Data

• CBC- WNL
• BMP- WNL
• UA- WNL
• CSF opening pressure - unknown
• WBC 2 , RBC 3
• Glucose 51, protein 35
• Gram stain no organism
• Culture- NGTD

8
Diagnostic Data

• HIV Ab- Non reactive for HIV 1 and 2.

9
Radiographs

• CT BRAIN with/without contrast
• -No acute abnormality
• CXR- Bibasilar subsegmental
• atelectasis versus scarring.

10

• Dxd was probable sulfa allergy.
• Sulfadiazine was changed to clindamycin
• Pt was D/Cd home in 2 days.

11
(No Transcript)
12
(No Transcript)
13
(No Transcript)
14
(No Transcript)
15
(No Transcript)
16
(No Transcript)
17
Negative IFA for antibodies to T. gondii
This is a positive reaction (tachyzoites human
antibodies to Toxoplasma FITC-labelled
antihuman IgG fluorescence.)
18
Toxoplasma gondii tachyzoites, Giemsa stain
Tachyzoites  are typically crescent shaped with a
prominent, centrally placed nucleus.
19
(No Transcript)
20
UVEITIS

• Anterior uveitis
• - iritis
• Symptoms
• - pain
• - redness

21
UVEITIS

• Posterior uveitis
• - retinitis
• - choroiditis
• - vitritis
• - intermediate uveitis
• - pars planitis
• - retinochoroiditis

22
Posterior uveitis

• Diagnosed by
• Direct visualization
• And/or by detecting leukocytes in the vitrous
  humor
• Symptoms
• Painless
• Visual changes floaters

23
ETIOLOGY
24
(No Transcript)
25
(No Transcript)
26
(No Transcript)
27
Infectious Causes

• CMV
• Found almost exclusively in immunocompromised
  host, esp pts with AIDS ( low CD4 count)
• Syphilis
• Tuberculosis
• Extremely uncommon cause in US
• Cat scratch disease

28
Ocular Toxoplasmosis

• Most common cause of posterior uveitis in
  immunocompetent individuals.
• 25 of posterior uveitis cases in the US.
• gt85 of posterior uveitis cases in southern
  Brazil.
• Glasner PD et al. An unusually high
  prevalence of ocular toxoplasmosis in southern
  Brazil.Am J Ophthalmol. 1992 Aug
  15114(2)136-44.
• Congenital or post-natally acquired.
• May occur during acute or latent stage.

29
Ocular Toxoplasmosis

• Patients who present with chorioretinitis as a
  late sequela of the infection acquired in utero
  are more frequently in the second and third
  decades of life.
• Bilateral disease, old retinal scar, and
  involvement of macula.

30
Ocular Toxoplasmosis

• Patients who present with chorioretinitis as an
  acute infection are more often between the
  fourth and sixth decades of life.
• Often unilateral involvement.
• Usually spare macula, not associated with old
  scars.

31
Ocular Toxoplasmosis

• Complete or partial loss of visual acuity.
• Localized necrotizing retinitis
• headlight in the fog white retinal lesion
  can be seen through a dense vitreitis.

32
Ocular Toxoplasmosis

• Atypical clinical and serologic manifestations
  found most commonly in the elderly and
  immunocompromised pts.
• In pts with atypical lesions or an inadequate
  clinical response to therapy or
• other diagnostic procedures are not
  helpful-should consider send vitreous fluid for
  PCR.

33
Diagnosis

• Clinical features
• Serology may be helpful.
• Negative serology help eliminating disease.
• Serial titer IgG, IgM 3 weeks intervals-recent
  acquired infection.
• IgA are detectable for only 7 months.

34
SEROLOGY

• Standard is Sabin-Feldman dye test.
• ELISA, IFA
• False positive ELISA
• - Patients with Rheumatoid factor, ANA
• PCR in ocular tissue, intraocular fluid

35
Treatment

• Often a self-limited process in immunocompetent.
• Criteria for initiation of treatment
• - Lesion in temporal arcade
• - Affect optic nerve
• - Moderate to severe vitreous inflammation

36
Treatment

• Relative indication
• Lesion with active inflammation gt 1 month
• Multiple active lesions
• Newly acquired lesions

37
124 triple therapy, 1234 quadruple
therapy
38

• Other agents
• - Atovaquone
• - Spiramycin
• - Azithromycin
• - Minocycline

39
Treatment

• Stanford MR, et al. Antibiotics for toxoplasmic
  retinochoroiditis an evidence-based systematic
  review. Ophthalmology. 2003 May110(5)926-31
  quiz 931-2.
• Gilbert RE, et al. Antibiotics versus control for
  toxoplasma retinochoroiditis.Cochrane Database
  Syst Rev. 2002(1)CD002218.
• Lack of evidence to support routine antibiotic
  treatment for acute toxoplasmic
  retinochoroiditis.

40

• Placebo-controlled randomized trials of
  antibiotic treatment in patients presenting with
  acute or chronic toxoplasmic retinochoroiditis
  arising in any part of the retina are required.