| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Brief Communication |
Correspondence: 1Corresponding Author: Dr. Jairo Nunes, Department of Veterinary Pathobiology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4467
 |
Abstract |
|---|
 TOPSources and manufacturers Abstract References |
|---|
Key Words: Histoplasma capsulatum • horse • mesenteric lymph nodes • small intestine
Histoplasmosis in horses may result from infection by 2 distinct species of the genus Histoplasma, namely H. capsulatum and H. farciminosum.1,3,4,5,7,11–15 Histoplasma farciminosum is the etiologic agent of epizootic lymphangitis, which has not been reported in the Western hemisphere.8 Histoplasma capsulatum is a dimorphic fungus that grows intracellularly as a yeast form with an affinity for cells of the monocytic-macrophage system. The mycelial form of the fungus grows naturally in soil.15 H. capsulatum has a worldwide distribution, with the highest prevalence of infection along the Mississippi and Ohio river valleys of North America.15 Horses appear to be relatively resistant to histoplasmosis,7,15 with far fewer reported cases than in humans, dogs, or cats.7 Previous reports of equine histoplasmosis have described localized infections of lungs;3,9,15 bone marrow;15 placenta;6,15 eyes;15 and colon, cecum, and mesenteric lymph nodes.4 A single case of disseminated histoplasmosis that involved lung, pleura, spleen, kidney, liver, small intestine, and colon has been reported.7
A 3.5-year-old Thoroughbred mare was presented to the Department of Large Animal Medicine and Surgery at Texas A&M University with a 2-month history of anorexia and weight loss, and a 2-week history of abdominal discomfort. At presentation, the mare was depressed and in poor body condition (weight, 376 kg). Before presentation, the mare had been treated with ivermectin,a psyllium husk,b and mineral oil. A complete blood count (CBC) and a serum biochemical analysis were performed. The CBC revealed a mild anemia, with hemoglobin, 9.69 g/dl (11–19 g/dl), and hyperfibrinogenemia, 500 mg/dl (100–400 mg/dl). Serum biochemical analysis revealed hypoalbuminemia, 2.2 g/dl (2.3–3.1 g/dl); hyperglobulinemia, 4.4 g/dl (2.2–3.8 g/dl); hyponatremia, 131 mmol/liter (132–141 mmol/liter); hypochloremia, 96 mmol/liter (98–105 mmol/liter); hyperphosphatemia, 5.4 mg/dl (1.7–3.9 mg/dl); and low ionized calcium, 6.25 mg/dl (6.61–7.30 mg/dl). Other hematologic and biochemical values were within normal limits. Rectal examination and abdominal ultrasonography revealed a large, firm, lobulated mass in the caudal abdomen around the level of the left kidney. Abdominal neoplasia was suspected, and the animal was euthanized and submitted for necropsy.
Gross lesions of significance were limited to the abdominal cavity, which contained approximately 1 liter of a serosanguineous effusion. A firm, encapsulated, multilobulated mass, which measured 23 x 20 x 18 cm, was present at the root of the mesentery (Fig. 1). On the cut surface, this mass contained multiple yellow, friable caseous foci surrounded by a 0.5–1-cm-thick fibrous capsule. A similar 5-cm diameter mass was adjacent to the left adrenal gland. Mesenteric, cecal, and colonic lymph nodes were markedly enlarged (up to 10 cm in diameter), and contained necrotic foci on the cut surface similar to those described in the mesenteric root mass. The mucosa and the submucosa of the ileum contained numerous, single to coalescing dark red raised nodules, 0.5–3 cm in diameter, which contained a central umbilicated area (Fig. 2). The intestinal mucosa between these nodules was diffusely reddened. The nodules were distributed circumferentially, but were most numerous along the antimesenteric aspect of the small intestine. While these nodules extended to the duodenum, they became progressively less prominent and less numerous proximal to the ileum. There were no gross abnormalities in the lungs or thoracic lymph nodes. Sections of multiple tissues were fixed in neutral buffered 10% formalin, were processed routinely, sectioned at 5 µm, and stained with hematoxylin and eosin (HE), periodic acid–Schiff (PAS), Grocott methenamine silver (GMS), and Gram stains. A sample of 1 small-intestinal nodule was submitted for fungal culture. Sabouraud dextrose agar was inoculated and incubated at room temperature for 5 weeks.
|
Two sections of the small-intestinal lesions were immunostained with a polyclonal antibody against Histoplasma spp. by using a labeled streptavidin-biotin peroxidase technique previously described.10 Positive controls consisted of H. capsulatum infected tissues, and the primary antibody was replaced by buffer for negative controls. The vast majority of intracellular organisms stained positively for Histoplasma spp. in all sections tested (Figs. 5, 6). No significant pathogenic fungi were isolated from the small-intestinal nodule.
A diagnosis of abdominal histoplasmosis was made based on the gross, microscopic, and immunohistochemical findings. This case is remarkable for the size and the extent of the abdominal lesions. To the authors' knowledge, this is the first report of histoplasmosis that presented as a large intra-abdominal mass in a horse. The most likely etiologic agent is H. capsulatum. There was no history of overseas travel to suggest infection with Histoplasma farciminosum.
Failure to culture Histoplasma spp. from this horse may be attributable to the collection of inadequate samples (no organisms in the tissues sampled for fungal culture), inappropriate culture techniques, or inadvertent mishandling of the sample.
Disseminated histoplasmosis is observed most frequently in dogs,8 where risk factors include exposure to high numbers of organisms, young age, and possible immunological compromise.2 In humans, disseminated histoplasmosis is rare and occurs mainly in patients who are immunologically compromised, especially those with human immunodeficiency virus infection.15 In a previous report of disseminated histoplasmosis in a horse that involved lungs, bone marrow, eyes, placenta, and intestine, as well as mesenteric lymph nodes, prolonged administration of dexamethasone was suggested to have resulted in immunological compromise.7 In the present case, the organism had also disseminated throughout the small-intestinal mucosa and into several abdominal lymph nodes. Rare organisms were also observed in the liver, but lesions were limited to the abdominal cavity. No predisposing factors were identified, and there was no specific evidence of immunosuppression or histologic evidence of lymphoid depletion in the spleen. Serologic testing for equine infectious anemia virus was not performed.
Animals become infected with Histoplasma usually via inhalation of spores from contaminated soil.2,5,8 The infection is initially established in the lung where the spores develop into the yeast form, which are phagocytosed by pulmonary macrophages and subsequently may gain access to the circulation and disseminate to various organs.8,15 Alternatively, Histoplasma organisms might be coughed up and swallowed, thereby exposing the gastrointestinal tract to the organism.5 A further possibility is that primary gastrointestinal infection may occur in the absence of detectable pulmonary lesions, as suggested in a report of granulomatous colitis in a horse.4 In the present case, there was no clinical history of respiratory disease and no gross or histologic evidence of current or previous pulmonary infection with Histoplasma spp., which suggests the route of infection may have been oral.
|
Acknowledgments |
|---|
|
Sources and manufacturers |
|---|
|
TOPSources and manufacturersAbstractReferences |
|---|
a. Zymectin, Merial Limited. Duluth, GA.
b. Metamucil, The Procter and Gamble Co., Cincinnati, OH.
|
References |
|---|
|
TOPSources and manufacturersAbstractReferences |
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
