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Journal of Clinical Microbiology, June 1999, p. 2102-2103, Vol. 37, No. 6
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Scopulariopsis chartarum Systemic
Mycosis in a Dog
Ronald D.
Welsh* and
Ray W.
Ely
The Oklahoma Animal Disease Diagnostic
Laboratory, College of Veterinary Medicine, Oklahoma State University,
Stillwater, Oklahoma 74078
Received 30 December 1997/Returned for modification 9 April
1998/Accepted 20 January 1999
 |
ABSTRACT |
Scopulariopsis chartarum was reported as the agent of a
multisystemic infection in a dog. The clinical syndromes in this dog with a fulminating mycotic disease mimicked those observed in dogs
infected with canine distemper virus.
 |
CASE REPORT |
A 2-year-old, mixed-breed, male dog
that had been captured by animal control officials was presented to the
Oklahoma Animal Disease Diagnostic Laboratory for euthanasia and
diagnostic tests. The dog was initially found to be dehydrated, and the
animal had diarrhea over the first 10 days of laboratory confinement.
The course worsened to episodes of myoclonia and convulsions. The dog
displayed "chewing gum fits" and other nervous disorders and ultimately advanced to a comatose state which caused the kennel personnel to request that the animal be euthanized. The clinical diagnosis was infectious canine distemper.
At necropsy, the predominant lesions discovered were enlarged kidneys
with a purulent exudate in the renal pelvis and scattered, 3- to 4-mm
yellow foci in the renal parenchyma and raised 1- to 3-cm splenic
plaques and white foci in the interventricular septum of the heart. The
meninges had 2- to 3-mm yellow foci, and there was an area of
liquefaction necrosis in the rostral area of the left cerebral
hemisphere. The gross postmortem conclusion was that the animal
displayed ascending pyelonephritis and septicemia which is not
consistent with infectious canine distemper.
Histopathologic examination revealed an area of necrosis and
hemorrhage surrounded by granulomatous inflammation in the splenic parenchyma. There was marked centrilobular hepatocellular fatty change
and midzonal cloudy swelling in the liver. Marked tubular and ductal
dilations were observed in the renal cortex and medulla. Numerous
pyogranulomatous foci were present in the renal cortical interstitium
with several small red infarcts in the renal cortex. Pyogranulomatous
and necrotizing foci were distributed throughout the renal parenchyma
(Fig. 1).

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FIG. 1.
Photomicrograph of a section of the kidney of the
studied animal. Note the pyogranulomatous inflammation and branched
septate hyphae. Gomori's methenamine-silver stain was used.
Magnification, ×486.
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|
As determined microscopically, the meninges were infiltrated with
neutrophils, lymphocytes, and macrophages. Multiple granulomas were
centered on blood vessels in the neuropil of the brain. A large area of
necrosis was observed rostral to the thalamus. Fibrinopurulent inflammation and edema were associated with the cerebral hemisphere, with several septate, branching hyphae observed in the areas of necrosis and granulomas (Fig. 2). The
histopathologic conclusion was that the animal displayed mycotic
granulomatous encephalitis, meningitis, myocarditis, nephritis, and
splenitis.

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FIG. 2.
Photomicrograph of a section of the brain of the studied
animal. Note the branching septate hyphae. Gomori's methenamine-silver
stain was used. Magnification, ×486.
|
|
Frozen sections of the lung, brain, and urinary bladder tested negative
for canine distemper virus by specific immunofluorescent staining
(Veterinary Medical Research and Development, Pullman, Wash.). Routine
cultures of kidney, urinary bladder, lung, liver, spleen, and cerebral
spinal fluid on blood agar at 37°C did not yield any bacteria. Cells
from the cerebral hemisphere were cultured on Sabouraud dextrose agar
and mycobiotic agar (Difco Laboratories, Detroit, Mich.) at 25°C, and
a filamentous fungus was isolated. Young colonies were white and
glabrous at 2 to 3 days and became brown and granular after 6 to 7 days
of growth. The reverse was tan with a brownish center. A slide culture
stained with lactophenol cotton blue showed branched penicillus-like
structures with chains of echinulate conidia (Fig.
3). The final, taxonomic
evaluation identified the organism as Scopulariopsis
chartarum (cataloged as UTMB 3307 by Michael McGinnis, UTMB
Mycology Identification Services, The University of Texas Medical
Branch at Galveston).

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FIG. 3.
Cylindric annellide and catenulate annellocondia of
S. chartarum. Differential interference contrast microscopy
was used. Magnification, ×1,000.
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S. chartarum infection of dogs has not been previously
reported in the literature. The pathogenesis of infection in this case is speculative due to the absence of clinical history. However, if the
mechanism for infection is similar to other filamentous, nondimorphic
mycoses in dogs, the portal of entry is the skin (5, 6).
Reports of brain abscesses in domestic animals due to fungal infections
are conspicuously deficient in the literature. Although rare, most
cases of mycotic brain infections are caused by Cladosporium spp., but the sources of infections were not determined in previous studies (2, 7). Likewise, in humans, mycotic brain abscesses are generally cerebral phaeohyphomycoses caused by
Cladosporium spp. (1).
There is a paucity of information on Scopulariopsis sp.
infections in humans and animals, but these fungi are known to infect the nails, and they are occasionally associated with infections of soft
tissue, bone, and lungs in immunocompromised people (4). Since members of the genus Scopulariopsis are common soil
fungi, it seems obvious that most infections of animals would be via the cutaneous route. A recent report regarding these infections in
humans suggests an invasive cutaneous or pulmonary route of infection
with the teleomorphic stage of Scopulariopsis spp.
(3).
 |
ACKNOWLEDGMENTS |
We thank Sam Crosby of Edmond, Okla., for referral of this case and
Roger Nieman and Lester Pasarell for expert technical assistance.
 |
FOOTNOTES |
*
Corresponding author. Mailing address: The Oklahoma
Animal Disease Diagnostic Laboratory, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078. Phone: (405) 744-6623. Fax: (405) 744-8612. E-mail: mich{at}okstate.edu.
 |
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Journal of Clinical Microbiology, June 1999, p. 2102-2103, Vol. 37, No. 6
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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