female domestic shorthair
cat (Felis catus).This cat had a history of tail
chewing, hair loss and recurring dermatitis
over the tail and caudodorsum, occurring since this cat was acquired as a kitten from
Florida. Affected areas of skin were alopecic
with erythema, crusted papules, plaques, and
nodules. There was limited to no clinical
response to treatment with fluoxetine,
topical antibiotics and regular flea
prevention and the cat deteriorated
following injections of depomedrol and
cefovecin. Following biopsy and initial
diagnosis, the cat underwent tail amputation;
however, the cat had recurring dermatitis
over the caudodorsum 3 weeks
postoperatively and was euthanized and
submitted for necropsy.
At necropsy, there were
two reddened, ulcerated areas over the
caudodorsum with variable brown crusts and
dried red-brown exudate. The caudal, larger
area of ulceration and crusting was
overlying a healing scar within the skin
(interpreted as part of the surgical site from
the previous tail amputation). The cranial,
smaller area of ulceration was not associated
with the previous surgical wound. On cut
section, these areas extended into and
expanded the subcutis, with poorly
demarcated, tan to pink, firm, multifocal to
coalescing nodules. There was no gross
involvement of the underlying vertebrae and
no gross evidence of spread to lymph nodes
or visceral organs.
examined was taken from the cranial,
smaller area of skin ulceration not associated
with the previous surgical wound. Underlying
a locally extensive area of ulcerated
epidermis and expanding the dermis and
subcutis, there is a poorly demarcated, nonencapsulated
infiltration of large numbers of
eosinophils, moderate lymphoplasmacytic
and histiocytic infiltrates and fewer
neutrophils, with extensive, multifocal areas
of eosinophilic necrotic and karyorrhectic
cellular debris. Within areas of necrosis,
there are small to moderate numbers of
predominantly negatively stained, extracellular,
10-15 µm diameter hyphae with
variably prominent round or bulbous
dilatations and intermittent right angle
branching. Areas of necrotic cellular debris
and inflammatory cellular infiltrate surround and isolate small aggregates of irregular,
eosinophilic collagen fibers (collagenolysis).
Special Stains: Staining with Grocotts methenamine silver (GMS) yielded moderate numbers of broad, thick-walled hyphae of varying diameters that are occasionally septate. Staining with PeriodicAcid-Schiff (PAS) highlights hyphae with similar morphology, albeit less prominently.
1. Skin, caudodorsum: Dermatitis,
panniculitis, steatitis and myositis,
eosinophilic and histiocytic, with lymphoplasmacytic
infiltrates, marked, locally
extensive, chronic with multifocal necrosis
2. Skin, caudodorsum: Ulceration, multifocal,
moderate to marked, chronic
Previous biopsy and
culture of the affected areas yielded scant
mold; further identified as Lagenidium sp.
by 18S/ITS (internal transcribed spacer)
nucleic acid amplification and sequence
analysis. Culture of necropsy samples was
unable to repeat isolation of Lagenidium
Fungal dermatitis/Lagenidium sp.
hyphae present in this case are consistent
with a recurrence of dermatitis associated
with Lagenidium sp., previously confirmed
in this cat by 18S/ITS nucleic acid
amplification and sequence analysis.
Members of the genus Lagenidium sp. are a
group of the Oomycetes, closely related to
Pythium sp. and often referred to as water
molds. Oomycetes are frequently pathogens
of plants, nematodes, and insect larvae; however, they are occasionally associated
with disease in mammals.2 The most widely
known Lagenidium species is Lagenidium
giganteum, a pathogen of mosquito larvae
that has previously been implemented as a
biologic control agent.2 Although stages of
oomycetes may be morphologically similar
to fungal hyphae, oomycetes are
phylogenetically distinct from fungi.7,8 In
contrast to fungi, the cell wall of oomycetes
contains cellulose and β-glucan rather than
, and the cell membranes lack
ergosterol.7 Oomycetes also differ from
fungi with respect to life stages produced,
including the production of sporangia and
Most case reports of lagenidiosis involve
dogs; however, there have been several
recent reports in cats.7 Infection with
Lagenidium sp. in dogs typically occurs in
young to middle-aged dogs and most
frequently occurs in southeastern United
States.2,3,7 Exposure to water bodies such as
lakes and ponds is frequently, but not
always, reported.3 Recent molecular work
has led to the description of two closely related pathogens in dogs; Lagenidium
giganteum forma caninum and Paralagenidium
giganteum forma caninum causes cutaneous
or subcutaneous disease with frequent widespread
dissemination, involving visceral
organs, lymph nodes and/or great vessels.3
Paralagenidium karlingii infection in dogs
results in chronic ulcerative and/or nodular
dermatitis that does not typically
disseminate.5 Recommended treatment for
lagenidiosis is wide surgical resection where
possible.1,3,7 Prognosis is poor for
disseminated disease, with lagenidiosis
poorly responsive to medical therapy.2,9
Differential diagnoses for lagenidiosis on clinical presentation and histopathology may include pythiosis, resulting from infection with the oomycete, Pythium insidiosum; and zygomycosis, involving infection with fungal organisms such as Basidiobolus ranarum and Conidiobolus spp..1,2,5 All may result in granulomatous and/or eosinophilic inflammation and morphologically appear as broad, irregular branching hyphae that are rarely to occasionally septate.1 Differentiation is clinically important due to differing treatment and prognosis7,8.
Diagnosis of lagenidiosis can be challenging. Cytology and histopathology yield hyphae with similar morphology to pythiosis and zygomycosis.4 Although there may be subtle differences in size and/or morphology of hyphae, histopathology cannot be used for definitive differentiation.3 Fungal culture is possible but can be difficult due to the fastidious nature of Lagenidium sp. (particularly the sexual stages). Definitive diagnosis requires confirmation through molecular assays on tissue or cultured isolates.3,7,9 Lagenidium sp. should be considered a differential in cats with granulomatous to eosinophilic, nodular to ulcerative dermatitis.
Haired skin and subcutis:
Dermatitis, panniculitis and myositis,
eosinophilic and gran-ulomatous, and
extensive, marked, with
ulceration, and fungal
hyphae, domestic shorthair,
contributor provides an
excellent example and
overview of the pathogenic
Oomycete water mold,
Lagenidium sp. As mentioned
above, Lagenidium sp.
is strikingly similar in
clinical, and histologic
appearance to the more
6 As a result, the majority of conference participants had
pythiosis as their top differential for this
Infection with both Pythium insidiosum and Lagenidium spp. typically, but not always, occurs when the host has prolonged contact with standing or stagnant water containing the motile aquatic flagellate zoo-spores.2,3,6 This infectious form of the organism is attracted by animal fur, damaged skin, and intestinal mucosa. As a result of contact with standing water, infections in domestic animals are most commonly reported in the limbs, ventral thorax, and abdomen. When a mammalian host with a skin injury enters a contaminated pond, the oomycete zoospores of will encyst upon contact with the injured skin and mechanically penetrate the tissue, causing clinical disease.6
Like pythiosis, this disease is typically highly aggressive and lesions in the great vessels, mediastinum, lungs, and esophagus have been reported in dogs. However, unlike pythiosis, gastrointestinal disease has not been reported in Lagenidium spp.6Both entities are associated with a poor to grave prognosis even with wide surgical excision of cutaneous masses because the majority of animals infected with this pathogen have occult, non-resectable, disease in regional lymph nodes or distant sites when initially diagnosed. 2,3 In dogs infected with the less aggressive species, Paralagenidium karlingii mentioned by the contributor, surgery that achieves three cm margins is often curative.7 Medical therapy for lagenidiosis is typically ineffective because ergosterol, the target for most antifungal drugs, is lacking in the Oomycete cell membrane. 6,7
Conference participants discussed this lesion as a great example of chronic-active inflammation. Chronic-active inflammation occurs when the inciting inflammatory stimulus has not been removed from the chronic inflammatory process and continues to elicit an acute inflammatory response.1
1. Ackermann M. Inflammation and healing. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 4th ed. St. Louis, MO:Mosby Elsevier; 2012:127.
2. Grooters AM. Pythiosis, lagenidiosis and zygomycosis. Vet Clin Small Anim. 2003; 33:695-720.
3. Grooters AM, Hodgin EC, Bauer RW, Detrisac CJ, Znajda NR, Thomas RC. Clinicopathologic findings associated with Lagenidium spp. infection in 6 dogs: Initial description of an emerging oomycosis.J Vet Intern Med. 2003;17:637-646.
4. Grooters AM, Foil CS. Miscellaneous fungal infections. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 4th ed. Philadelphia, PA: WB Saunders; 2012:681-683.
5. Hartfield JN, Grooters AM, Waite KJ. Development and evaluation of an ELISA for the quantification of anti-Lagenidium giganteum forma caninum antibodies in dogs. J Vet Intern Med. 2014; 28:1479-1484.
6. Mauldin E, Peters-Kennedy J. Integumentary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmers Pathology of Domestic Animals. Vol 1. 6th ed. Philadelphia, PA:Elsevier; 2016:657-660.
7. Mendoza L, Vilela R. The Mammalian pathogenic oomycetes. Curr Fungal Infec Rep. 2013; 7:198- 208.
8. Raffaele S, Kamoun S. Genome evolution in filamentous plant pathogens: why bigger can be better. Nature Reviews Microbiology. 2012; 10:417-430.
9. Znajda NR, Grooters AM, Marsella R. PCR-based detection of Pythium and Lagenidium DNA in frozen and ethanol-fixed animal tissues. Vet Dermatology. 2002; 13:187-194.