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1.
The aim of this study was to evaluate the prevalence of gastric Helicobacter-like organisms (GHLO) and gastritis in the gastric mucosa of dogs with gastric disorders. Tissue samples of the gastric mucosa were obtained from 30 dogs with gastrointestinal symptoms (vomiting, abdominal pain or discomfort, loss of appetite) during endoscopy. Histopathological examinations were performed and occurrence of GHLO infection, gastritis and other mucosal changes were estimated. The GHLO infection and gastritis were identified in 63.3 and 36.6% of dogs respectively; other mucosal changes included fibrosis in the lamina propria, degenerative changes of the gastric glands and hyperplasia of the parietal cells. The present study has revealed that microscopically found gastritis is not frequent in dogs examined by endoscopy. GHLO infection can be responsible for some cases of gastritis and hyperplasia of parietal cells in dogs.  相似文献   

2.
Preliminary evidence for the presence of Helicobacter-like bacteria was sought in 395 porcine gastric samples by a urease test. Of the samples, 37% (146/395) were urease-positive and 82% (82/100) of the Gram-stained urease-positive samples showed large, tightly spiralled organisms. Several methods were applied to culture the organisms but isolation was unsuccessful, contaminant organisms being considered to be one of the major problems. PCR with Helicobacter genus-specific primers for 16S rRNA and ureB genes, and primers for H. pylori vacA and cagA genes were tested with 102 urease-positive biopsy samples. The PCR results showed some evidence for the presence of the urease and the vacA genes in porcine Helicobacter-like bacteria and raises the possibility of pathogenicity by these organisms.  相似文献   

3.
The aim of this study was the evaluation of gastric epithelial cell proliferation rate in connection with the gastric Helicobacter-like organisms (GHLO) infection in dogs. The study was performed on samples of the gastric mucosa obtained during necropsies from 60 dogs euthanasized for various reasons. Microscopic preparations were stained with the hematoxylin-eosin method, Giemsa method, Warthin-Starry silver method and immunohistochemical method (MIB-1 antibody) to investigate the expression Ki67 antigen. In glands of the gastric body and antrum different proliferation patterns were observed. The gastric epithelial cell proliferation rate in the gastric antrum was significantly higher in dogs with GHLO colonization in relation to dogs without GHLO, and in the gastric body was significantly higher in dogs with mild GHLO colonization as compared to dogs with significant GHLO colonization and without GHLO colonization. The gastric epithelial cell proliferation rate in the gastric body was significantly higher in dogs with gastritis in comparision with the dogs without gastritis irrespectively from the presence or absence of the GHLO colonization. It seems that the presence of the GHLO colonization, as well as the inflammatory state in the gastric mucosae, can alter the rate of the gastric epithelial cells proliferation in dogs.  相似文献   

4.
The objective of this study was to improve the visual localization of urease activity of Helicobacter pylori-like organisms (HPLO) on swine gastric mucosa by in vitro optimization of the urea concentration and pH indicator of a urease test reagent. Five 21-day-old conventional pigs were infected orally with HPLO (3 pigs) or Brucella broth alone (2 pigs). At 17 d after infection the pigs were euthanized and their stomachs excised and tested for HPLO by a modified urease test formulation sprayed onto the gastric mucosa, as well as confirmatory culture and isolation of HPLO from urease-positive sites. This study showed improved detection of HPLO in porcine gastric mucosa with the use of a modified urease test formulation containing 5% urea and the pH indicator bromocresol purple compared with the use of a conventional formulation of 2% urea and phenol red. This test can readily be applied to achieve a presumptive diagnosis of HPLO in cases of gastritis or gastric esophageal ulceration in pigs.  相似文献   

5.
Archival specimens of gastric mucosa of 10 raccoons (Procyon lotor), 9 porcupines (Erethizon dorsatum), 6 grey foxes (Urocyon cinereoargenteus), 6 bobcats (Lynx rufus), 4 skunks (Mephitis mephitis), and 3 black bears (Ursus americanus) were microscopically examined for evidence of Helicobacter-like organisms. Such organisms were seen in the specimens from the grey foxes and bobcats only. Histochemical stains (modified Steiner and carbol fuchsin methods) revealed long spiral organisms within lumina of gastric glands; however, neither gross nor microscopic lesions were observed. By electron microscopy (EM), the organisms were found to be free in the glandular lumina and were seen occasionally in the cytoplasm of gastric epithelial cells. Morphologically, 2 different phenotypes of spiral organisms were identified by EM. The organisms associated with bobcats appeared to be more tightly coiled than those seen in grey foxes. The presence of Helicobacter-like organisms in the gastric mucosa of grey foxes has not previously been described.  相似文献   

6.
The discovery of the spiral bacterium Helicobacter pylori and its causative role in gastric disease in humans has brought a dramatic change to gastroenterology. Although spiral bacteria have been known for more than a century to infect the stomachs of dogs and cats, recent research has been conducted mainly in the wake of interest in H. pylori. H. pylori has not been found in dogs and only very rarely in cats and zoonotic risk is minimal. A variety of other Helicobacter spp. can infect the stomach of pets; however, their pathogenic role is far from clear, and they have a small but real zoonotic potential. The prevalence of gastric Helicobacter spp. in dogs and cats is high, irrespective of clinical signs, and as in human medicine, mode of transmission is unclear. The relationship of Helicobacter spp. to gastric inflammation in cats and dogs is unresolved, with inflammation, glandular degeneration, and lymphoid follicle hyperplasia accompanying infection in some but not all subjects. Circulating anti-Helicobacter immunoglobulin G antibodies have been detected in 80% of dogs with naturally acquired infection and most dogs and cats with experimental infection. The gastric secretory axis is similar in infected and uninfected cats and dogs and no relationship of infection to gastrointestinal ulcers has been found. Differences in the pathogenicity of Helicobacter spp. are apparent, because infection with H pylori is associated with a more severe gastritis than infection with other Helicobacter spp. in both cats and dogs. Rapid urease test, histopathology, and touch cytology are all highly accurate invasive diagnostic tests for gastric Helicobacter-like organisms in dogs and cats, whereas culture and polymerase chain reaction are the only means to identify them to the species level. Urea breath and blood tests or serology can be used to diagnose Helicobacter spp. noninvasively in dogs and cats. Most therapeutic studies in pets have not shown long-term eradication of Helicobacter spp. Whether this is due to reinfection or recrudescence has not been established.  相似文献   

7.
OBJECTIVE: To determine whether 2 isolates of recently isolated swine-origin Helicobacter pylori-like bacteria are pathogenic in pigs and compare the signs of gastric disease induced by these isolates with those detected in H pylori- and Helicobacter heilmannii-infected pigs. ANIMALS: 36 neonatal gnotobiotic pigs. PROCEDURE: Groups of separately housed pigs were inoculated orally with swine-origin Helicobacter-like isolates 2662 or 1268, H pylori (human gastric pathogen), or a gastric homogenate from gnotobiotic swine containing H heilmannii. Noninoculated pigs were used as control animals. Clinical signs and development of homologous and heterologous antibodies against Helicobacter organisms were assessed. After euthanasia, gastric tissues were examined grossly and microscopically; Helicobacter organisms were detected by use of Warthin-Starry and immunohistochemical stains. RESULTS: Both porcine Helicobacter-like isolates colonized the stomachs of swine. Isolate 2662 was highly pathogenic; in 13 isolate 2662-inoculated pigs, gastroesophageal ulcerations developed in 9 and ulceration of the gastric glandular mucosa was detected in 5. Histologically, inflammatory gastritis consisting of multifocal to diffuse lymphocytic and plasmacytic cellular infiltrates and lymphoid follicle formation in the gastric lamina propria accompanied bacterial colonization of the gastric compartment. In contrast, H heilmannii was minimally pathogenic in that only modest inflammatory cell infiltrates were seen. Gastroesophageal or mucosal ulcers were not evident in pigs inoculated with H heilmannii. CONCLUSIONS AND CLINICAL RELEVANCE: These data indicate that swine-origin H pylori-like bacteria can be pathogenic in pigs and suggest that porcine gastric disease may be mediated, in part, by colonization of the stomach by swine-origin H pylori-like bacteria.  相似文献   

8.
ABSTRACT: In dogs Helicobacter spp. are found in all gastric regions usually localized in the surface mucus, gastric glands and parietal cells. The aim of this study was to detail the distribution of Helicobacter spp. in the fundic mucosa of asymptomatic Beagle dogs and their intracellular localization within parietal cells, in order to evaluate species-specific pathogenetic effects on gastric cells. The presence of Helicobacter spp. was investigated by immunohistochemistry, TEM, and PCR in the fundic mucosa of six Beagle dogs. Helicobacter spp. were found in all dogs examined, and H. bizzozeronii and H. felis were identified by PCR and confirmed by TEM. In the lumen of the fundic glands, co-localization was common. H. bizzozeronii was present in larger numbers than H. felis in both intraluminal and intraparietal localization. The amounts of H. bizzozeronii were similar in superficial and basal portions of the glands. H. felis was predominantly localized in the superficial portions of gastric glands but almost absent from the base. Within parietal cells, most Helicobacter organisms were intracanalicular, but intact and degenerate Helicobacter organisms were also visualized free in the cytoplasm or in secondary lysosomes. No specific degenerative lesions were found in infected parietal cells. Helicobacter organisms were also observed within macrophages in the lamina propria. In conclusion, there is a differential distribution of H. bizzozeronii and H. felis in the fundic mucosa of Beagle dogs, and their intracellular localization in parietal cells and macrophages suggests novel pathogenic scenarios for the development of immune response and maintenance of chronic gastritis in dogs.  相似文献   

9.
The relationship of Helicobacter felis, an organism that is observed in the stomachs of dogs, to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter felis infection alters gastric morphology and gastric secretory function in dogs. Five specific-pathogen-free (SPF), Helicobacter-free Beagle dogs were examined before and for 26 weeks after inoculation with H. felis (ATCC 49179). Three SPF uninfected dogs served as controls. All five dogs became colonized by H. felis as determined by urease activity, histopathology, polymerase chain reaction, and transmission electron microscopic examination of serial gastric biopsies. The degree of colonization ranged from < 1 organism/400 x field to > 10 organisms/400 x field. The fundus, body, and cardia were most heavily colonized. Evaluation of gastric biopsies showed mild gastric inflammation and lymphoid follicles in both infected and uninfected dogs. There was no correlation between the number of organisms observed and the degree of gastric inflammation or number of lymphoid follicles. The gastric secretory axis, assessed by fasting and meal-stimulated plasma gastrin, mucosal gastrin and somatostatin immunoreactivity, fasting gastric pH, and pentagastrin-stimulated gastric acid secretion, was similar in both infected and uninfected dogs. Fasting gastric pH was not a reliable indicator of gastric secretory function. These findings suggest that H. felis may not be a gastric pathogen in dogs. However, the density of colonization and limited duration of infection should be considered when interpreting these findings.  相似文献   

10.
Light and electron microscopic and microbiologic evaluations were performed on mucosa of stomachs from 120 healthy slaughtered pigs. Helicobacter pylori was not found, but a tightly spiralled bacterium, not previously described, was seen in histological sections and/or in carbol fuchsin stained smears in 13 (10.8%) stomachs. In paraffin sections stained with carbol fuchsin, the bacteria were seen in the mucus of the lumen of the antral pits and in the mucosa surface within and beneath the mucus. In this sections of Polilyte embedded tissue the bacteria had three to eight spiral turns per cell (mean = five), flattened ends, a Gram-negative cell-wall structure and a sheathed flagella. The urease test was positive in gastric mucosa of 13 bacteria-positive pigs (10.8%). The microorganism was not cultured and did not cross-react with polyclonal antibodies raised in rabbits against H. pylori. Superficial chronic gastritis and "borderline" gastritis were observed in antral mucosa of 10 (76.9%) and of two (15.4%) spiral bacteria-positive pigs, respectively.  相似文献   

11.
Helicobacter-like organisms as well as fermentative bacteria have been implicated in gastric ulcer production in swine. Irregular feeding schedules are also considered a major risk factor. A research trial was conducted to determine whether medication with an acid secretion inhibitor (lansoprazole), either alone or in combination with an antibiotic (azithromycin), would protect pigs from gastric ulceration if the animals were subjected to a 48 h period of fasting. In a 2 x 3 factorial design, 48 pigs were fasted, while an equal number were fed ad libitum. Within these 2 study groups, pigs were randomly assigned to 1 of 3 treatments: control, 30 mg lansoprazole s.i.d. for 7 d, or lansoprazole (30 mg s.i.d. for 7 d) and azithromycin (500 mg s.i.d. for 3 d). Overall, fasted pigs were 1.9 times more likely to develop erosive or ulcerative lesions of the pars esophagea (chi2 = 9.89, P < 0.002). Treatment with an acid secretion inhibitor alone or in combination with an antibiotic did not protect pigs from developing gastric lesions. Helicobacter-like organisms were not detected in any of the stomachs. Possibly, the lansoprazole dose of 30 mg given once per day was insufficient to prevent pH levels from becoming low enough to cause damage to epithelial tissue. Alternatively other substances such as bile acids may have caused the ulcerative lesions, even though stomach acid production was suppressed.  相似文献   

12.
Nine helicobacter-positive pet dogs with upper gastrointestinal signs were studied to evaluate the effect of a triple therapy, normally applied to humans for the eradication of gastric helicobacters, on clinical signs and gastric histology, as well as the recurrence of helicobacters after eradication in an extended follow-up in four dogs. Endoscopy was performed at entry to the study and repeated after eradication therapies and additional treatments. If the triple therapy (amoxycillin, metronidazole and bismuth subcitrate) failed, tetracycline and omeprazole were prescribed. Additional therapies were instituted if clinical signs persisted after eradication therapies. Helicobacter status was verified from gastric biopsy specimens by the urease test and histological examination, and in a few dogs also by brush cytology. Triple therapy eradicated gastric helicobacters in 7/9 dogs; gastric helicobacters were also eradicated in one dog treated with tetracycline and omeprazole. Eradication of helicobacters resulted in significant improvement, but not total resolution, of clinical signs. Subsequent additional therapies resulted in further alleviation of clinical signs. Neither triple therapy nor additional therapies had a significant effect on gastric histological changes. Gastric helicobacters recurred in 4/4 dogs within three years of the eradication treatment. Because canine gastric helicobacters alone were not definitively shown to induce clinical signs, routine eradication therapy seems not to be warranted at present.  相似文献   

13.
We assessed gastric and intestinal permeability and performed gastroscopy to evaluate the effects of sustained strenuous exercise on the gastrointestinal tract in racing sled dogs. Three teams of racing Alaskan sled dogs were examined approximately 1 week before and 24 hours after the 2003 Iditarod sled dog race (1,100 miles in 10 days). Each examination consisted of the administration of a solution of sucrose, lactulose, and rhamnose to evaluate gastric and intestinal permeability, as well as gastroscopy to visually inspect the gastric mucosa. Of the 54 dogs examined before the race, 16 completed the course and contributed data to the analysis. Sustained strenuous exercise was associated with an increased frequency of gastric erosions or ulcerations seen endoscopically (0% prerace versus 61% postrace). A significant postrace increase occurred in the median lactulose to rhamnose ratio in both serum and urine (0.11 versus 0.165, P = .0363; 0.11 versus 0.165, P = .0090, respectively). No significant differences were found in median serum or urinary sucrose concentrations when pre- and postrace values were compared. No correlation was found between visible gastric lesions and the concentration of sucrose in serum or urine samples obtained 4-5 hours after administration of the sugar solutions. We conclude that sustained strenuous exercise is associated with increased intestinal permeability, but the sucrose permeability test as we performed it did not correlate with visible gastric lesions.  相似文献   

14.
Five gnotobiotic Beagle dogs were orally inoculated with a pure culture of Helicobacter felis. The remaining two littermates served as contact controls. Thirty days after infection, all animals were euthanatized and specimens were collected for evaluation. In infected dogs, H. felis was recovered from all areas of the stomach. Colonization was heaviest in the fundus and antrum. H. felis was not cultured from any segment of the gastrointestinal tract distal to the duodenum. Two weeks after infection, all five infected dogs had detectable IgM and IgG serum antibody to H. felis, whereas control dogs had no measurable H. felis serum antibody throughout the study. Histopathologic changes in the stomachs of infected dogs included large numbers of lymphoid nodules throughout all regions of the gastric mucosa and were most numerous in the fundus and body. A mild, diffuse lymphocytic infiltrate with small numbers of plasma cells and eosinophils was also present in the subglandular region of all portions of the gastric mucosa. Electron microscopic examination revealed large numbers of spiral-shaped H. felis in gastric mucus adjacent to or superimposed over the areas of inflammation. Occasionally, however, H. felis was observed within the canaliculi of gastric parietal cells. Histopathologic changes in the stomachs of the contact control dogs were limited to focal infiltrates of eosinophils and small aggregates of lymphocytes in the subglandular portions of the gastric mucosa in one animal. Infection with H. felis is a likely cause of naturally occurring lymphofollicular gastritis.  相似文献   

15.
Helicobacter-like organisms are frequently observed in the stomach of dogs but the relationship between these microorganisms and gastric pathology has not been clearly established. Different species of helicobacters are known to be present in the canine stomach but their specific prevalence in naturally infected dogs is unknown. The aims of this study were to isolate and characterize helicobacters in canine gastric biopsies, to compare the commonly used tests for the identification of Helicobacter spp. and to determine the occurrence of these species in dogs. Twenty-three out of 25 dogs (92%) were positive for Helicobacter-like organisms in cytological screening. Culture was successful from biopsies of 5/25 dogs. The isolates were analyzed by electron microscopy, biochemical and physiological tests, whole protein analysis and 16S rDNA sequencing. Helicobacter felis was identified in four samples and Helicobacter bizzozeronii in one sample. Only the whole protein analysis in combination with electron microscopy was able to clearly discriminate the two species. Compared to the high prevalence of Helicobacter-like organisms, the occurrence of H. felis and H. bizzozeronii, was low (17 and 4%, respectively). No Flexispira rappini-like organisms or H. salomonis were detected. Electron microscopy revealed that H. bizzozeronii-like microorganisms were present in three additional biopsies where we were unable to culture any Helicobacter-like organisms. These observations indicate that in the stomach of dogs not all helicobacters are culturable. The unculturable bacteria appeared to be the prevalent ones and may represent different spiral organisms. The presence of distinct helicobacters with different characteristics can reflect different roles in the pathogenesis of canine gastric disease.  相似文献   

16.

Background

Confocal endomicroscopy (CEM) is an endoscopic technology permitting in vivo cellular and subcellular imaging. CEM aids real‐time clinical assessment and diagnosis of various gastrointestinal diseases in people. CEM allows in vivo characterization of small intestinal mucosal morphology in dogs.

Objective

To determine the feasibility of CEM to evaluate gastric mucosal morphology in dogs and to characterize the appearance in healthy dogs.

Animals

Fourteen clinically healthy research colony dogs.

Methods

Experimental study. Under general anesthesia, dogs underwent standard endoscopic evaluation and CEM of the gastric mucosa. In the initial 6 dogs, fluorescent contrast was provided with the fluorophore acriflavine (0.05% solution), applied topically. Subsequently, 8 dogs were assessed using a combination of fluorescein (10% solution, 15 mg/kg IV), followed by acriflavine administered topically. For each fluorophore, a minimum of 5 sites were assessed.

Results

Confocal endomicroscopy provided high quality in vivo histologically equivalent images of the gastric mucosa, but reduced flexibility of the endoscope tip limited imaging of the cranial stomach in some dogs. Intravenous administration of fluorescein allowed assessment of cellular cytoplasmic and microvasculature features. Topical application of acriflavine preferentially stained cellular nucleic acids, allowing additional evaluation of nuclear morphology. Identification of Helicobacter‐like organisms was possible in 13 dogs.

Conclusion and Clinical Importance

Confocal endomicroscopy provides in vivo images allowing assessment of gastric mucosal morphology during endoscopy, potentially permitting real‐time diagnosis of gastrointestinal disease.  相似文献   

17.
The canine gastric mucosa is known to be a habitat for various Helicobacter species. So far, five Helicobacter species have been described from the canine gastric mucosa, but histological studies have demonstrated a greater variety. In order to gain more information on diversity of canine gastric mucosa colonising helicobacters, biopsy samples of four pet dogs were examined by DNA-based techniques. PCR with a primer pair binding specifically to the 16S rDNA of the species of the genus Helicobacter and generating a fragment of approximately 400 bp indicated the presence of Helicobacter strains in the stomachs of the four dogs. PCR products were cloned into Escherichia coli DH10B and PCR-re-amplified 16S rDNA fragments were subjected to amplified ribosomal DNA restriction analysis (ARDRA) employing restriction enzyme HhaI. Restriction profiles indicated the presence of at least two different Helicobacter species in two dogs. Partial sequences of 16S rDNA of six clones were compared with sequences available in the EMBL data bank. Two sequences obtained from different dogs were identical with the corresponding sequences of Helicobacter pylori strains. Three sequences showed highest but moderate similarity values to H. pylori (96.6-98.0%) and one sequence to Helicobacter salomonis (97.3%). In contrast to previous reports our data implicate that the gastric mucosa of dogs may be colonised by strains of H. pylori or a very closely related species but they also confirm indications for the presence of so far uncultivated species of Helicobacter.  相似文献   

18.
BACKGROUND: Alterations in the appearance and function of gastrointestinal mucosa are common after strenuous exercise. However, the duration of exercise required to alter the gastrointestinal mucosa has not been reported. HYPOTHESIS: We used 42 sled dogs to test the hypothesis that the magnitude of exercise-induced gastrointestinal mucosal dysfunction is related to exercise duration. ANIMALS: Six dogs served as conditioned controls, and the remaining dogs were randomly chosen for examination after 1-5 consecutive days of running at 100 miles/d. METHODS: Gastroduodenoscopy and measurement of gastric permeability were performed 24 hours after cessation of exercise. Intestinal protein loss (represented by fecal alpha-1 protease inhibitor concentration) was measured within 6 hours of cessation of exercise. Twelve of the 42 dogs were examined again after 5 months of detraining to determine the effect of training on gastrointestinal mucosal function. RESULTS: Exercise increased gastric permeability (P = .04) and endoscopic severity of gastric lesions (P < .0001), but neither variable was significantly affected by distance traveled. Acute exercise had no effect on intestinal protein loss. Untrained dogs had significantly lower fecal alpha-1 protease inhibitor concentrations compared with trained, unexercised dogs. Training had no effect on gastric permeability to sucrose or the endoscopic appearance of the stomach. CONCLUSIONS AND CLINICAL IMPORTANCE: These data suggest that relatively modest exercise is required to increase intestinal protein loss, but more substantial exercise is required to cause alterations in the proximal gastrointestinal tract. However, none of these alterations appear to progress with increasing exercise duration.  相似文献   

19.
The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.  相似文献   

20.
Blastomyces dermatitidis is a common etiologic agent of fungal pneumonia in dogs. Definitive diagnosis is based on cytologic demonstration of the organism in affected tissues. Fluid obtained through transtracheal aspiration has previously been reported to have a low diagnostic yield for B. dermatitidis organisms. This retrospective study identified B. dermatitidis organisms in 76% of samples when transtracheal aspiration was performed in 17 nonsedated dogs with pulmonary blastomycosis. Transtracheal aspiration is a noninvasive and simple procedure that should be considered as an early diagnostic test whenever blastomycosis is a differential diagnosis in dogs with pulmonary disease.  相似文献   

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