Imaging Features of Gastric Invasive Aspergillosis: A Report of Two Cases

Invasive aspergillosis is a rapidly progressive and highly lethal mycotic disease caused by Aspergillus species, usually Aspergillus fumigatus. The risk of this opportunistic infection is associated with the degree and duration of neutropenia. In particular, patients with severe neutropenia, a neutrophil count of less than 0.1 × 10³/µL, that has had a duration of more than 3 weeks, are considered a high-risk group (1). Although the airway is the most common portal of entry, there are a few rare reports of isolated small bowel infection without pulmonary involvement (2, 3, 4). However, Aspergillus infection of the gastric wall is extremely rare. In this report, we describe the CT findings in 2 patients with gastric invasive aspergillosis.

Aspergillus species are saprophytic molds that can cause a broad pathogenic spectrum. Over the decades, invasive aspergillosis has substantially increased and become of greater concern (5, 6). Invasive aspergillosis is usually acquired by inhalation. The extrapulmonary involvement of invasive aspergillosis is rare, but can involve the brain, sinus, kidney, liver, heart and pancreas. It has been reported that almost 25% of the patients with invasive pulmonary aspergillosis developed disseminated infection, and approximately 41-47% of these patients displayed gastrointestinal tract involvement (2). Although the lung is the usual portal of entry into the human host, isolated small bowel infections without lung involvement have been reported (2, 3, 4). The most commonly involved sites in the gastrointestinal tract are, in descending order, the oesophagus, colon, and small intestine (6). However, primary or disseminated gastric invasive aspergillosis is extremely rare. In addition, there have been only 2 reports describing imaging findings associated with gastric invasive aspergillosis. Yeom et al. (5) reported disseminated gastric invasive aspergillosis in a kidney-transplanted patient. They described the CT findings of a diffuse, low attenuating gastric wall thickening that was confirmed as a transmural infarction in pathological specimens. Trésallet et al. (7) reported a large defect of the posterior gastric wall potentially due to primary digestive aspergillosis.

In our first case, contrast-enhanced CT imaging showed nodular and irregular collections of intramural gas bubbles in the gastric fundus and body, representing emphysematous gastritis, and revealed decreased wall enhancement in those areas. Unlike Pseudomonas aeruginosa or Clostridium perfringens, Aspergillus is not a gas-forming pathogen, and thus, this pathogen is not a direct cause of emphysematous gastritis. This finding on imaging can be explained by the typical characteristics of invasive aspergillosis. A disseminated form or a direct insult of Aspergillus hyphae invades medium- or small-sized blood vessels, which results in the sequence of disturbed blood flow, thrombosis, necrosis, and haemorrhagic infarction. Alternatively, it is possible that gastric wall necrosis caused by invasive aspergillosis, could be followed by a gas-forming bacteria superinfection (8). Our first case was disseminated invasive aspergillosis that involved the stomach, spleen, and pancreas. In contrast, the second case was manifested on images as a presumed pseudoaneurysm in the anterior wall of the gastric body. However, this imaging feature can also be explained by the same pathophysiology. The second case might be localised invasive aspergillosis limited to a single organ, which is why there was no evidence of any other organ involvement upon imaging and no clinical manifestation except for gastric bleeding.

From the radiological point of view, considering the imaging findings in our first case, it is essential to differentiate this condition from benign gastric emphysema caused by aggressive vomiting, instrumentation, drug use, etc. Images of benign gastric emphysema reveal a thin, linear distribution of air running parallel to the border of the stomach (9). Contrary to gangrenous emphysematous gastritis, gastric wall thickening is unusual in benign gastric emphysema (9). In addition, it is very helpful to understand the patient's clinical situation, such as that of an immunocompromised host or recent clinical history. Emphysematous gastritis can be caused by gas-forming microorganisms, such as Streptococcus, E. coli, Pseudomonas aeruginosa, Clostridium perfringens, and Staphylococcus aureus (S. aureus). There are also extremely rare reports of invasive gastric mucormycosis with emphysematous gastritis (8). Although invasive aspergillosis usually occurs in severely neutropenic patients, it is very difficult to differentiate this condition from emphysematous gastritis resulting from gas-forming organisms or other fungi by imaging alone. Considering the differential diagnosis of gastric aneurysm, pseudoaneurysm can be caused by infection, and the most common causative pathogens are S. aureus and Streptococcus. Sometimes, pseudoaneurysm can occur due to trauma, post-operative complications, and pancreatitis. However, these aetiologies cannot be differentiated by imaging alone. The patient history and clinical situation must be considered and correlated.

Because positive blood cultures are infrequent, a biopsy is essential to visualise fungal hyphae by microscopic examination for confirmation of a diagnosis (5). However, amphotericin B or a second-generation triazole antifungal agent should be used upon the suspicion of the diagnosis because it is a highly fatal, rapidly progressive disease in immunocompromised patients. Unfortunately, in spite of systemic therapy, the prognosis is poor in patients with intra-abdominal visceral organ involvement (10).

In conclusion, gastric invasive aspergillosis may present as emphysematous gastritis or pseudoaneurysm in the gastric wall, especially in an immunocompromised host. A prompt work-up and early, accurate diagnosis are very important because this is a rapidly progressing, life-threatening infection.