This post will come from
the current issue of Clinical Laboratory Science (Spring 2014). If you receive
this journal, don’t cheat!
A 52 year old, healthy male
went on a scuba diving trip to Miami Beach, and returned with redness and
irritation in his right eye. He did wear contact lenses, and reported that he
felt an object was in his eye. His optometrist removed the foreign body from
his eye, and started the patient on vigamox and systane. It is important to
note that this patient did not possess any known risk factors:
immunosuprresion, host factors, and hospitalization.
After 48 hours, the patient’s
symptoms had worsened to increased redness, limited vision, and yellow
discharge from his right eye. He was referred to an ophthalmologist/corneal specialist
who collected corneal scrapings (Classmates: Always performed with a sterile platinum
scalpel). The patient’s results are below:
- Physical Assessment
- Superlative central infiltrate (an extreme permeation of the cornea, centrally located)
- Diffuse corneal haze
- Edema with 3-4+ conjuctival infection
- 1mm hypopyon (pus entering anterior chamber of eye)
- Corneal Scrapings
- Aerobic culture - negative
- Anaerobic culture - negative
- Fungal culture
- Day 3 – possible fungal forms; rare growth of mycelia fungal forms
- This specimen was then sent to a reference laboratory for identification
- Day 12 – causative agent growth confirmed
- Macroscopic – velvety, brown, cinnamon, buff/ orange-brown with radial folds; reverse appearance is white to brown
- Microscopic – small dome shaped vesicles (10-16 m), proximal (primary) phialides and shorter distal (secondary) phialides produce a "swept-forward" appearance; smooth conidia forming long chains
- 4 weeks – No additional fungi were isolated
The causative
agent is 1 of 20 Aspergillus species
capable of causing opportunistic infections in humans. It is found in soil,
decaying matter, household dust, building materials, and on plants. It is
commonly found in warm arable soils, particularly southern and southwestern
United States (unfortunately for us), and it is less common in forest areas
compared to cultivated solids.
The
typical defense against this agent is alveolar macrophages. This Aspergillus organism is more prone to
phagocytosis due to its surface high exposure of beta-1,3 glucan and
galactomannon. This organism remains viable after phagocytosed, but is unable
to germinate. It is also able to surve
in acidified phasgolysosomes.
Aspergillus sp produce two types of asexual
conidia (phialidic, accessory). One theory states that this organism’s
accessory conidia gives rise to its natural resistance. It is able to produce
accessory conidia directly on hyphae whether in vivo or in vitro. Accessory
conidia enhance virulence, germinate rapidly, enhance adherence to macrophages,
and are metabolically more active.
Definitive
identification of this organism and other fungal organisms are based on
microscopic findings (shape, conidia arrangement, existing structures). The
best technique to visualize these characteristics is the adhesive tape
preparation and addition of lactophenol cotton blue stain, wet mount, or
microslide culture. Another method possible for identification is real time
polymerase chain reaction (rt-PCR). This allows us to detect Aspergillus sp directly from biological
samples (plasma, serum, lung samples, bronchoalveolar lavage specimens, sputum,
aspirate fluid, thoracic puncture fluid, cerebral spinal fluid, liver tissue,
pericardial exudates) with as fast as same day analysis.
What is
the causative organism?
Aspergillus
niger
Aspergillus
terreus
Aspergillus
flavus
Aspergillus
fumigates
All
figures were retrieved from Clinical Laboratory Science Volume 27/Number 2 with
full reference to follow in next post.
