Abstract
Infectious esophagitis (IE) is the leading cause of esophagitis, second only to gastroesophageal reflux disease. Infectious esophagitis is typically observed in immunocompromised individuals due to neutropenia, HIV/AIDS, solid organ malignancies, cancer-directed therapy, or chronic steroid use. The most common causes of IE are herpes simplex virus (HSV), cytomegalovirus (CMV), and Candida albicans. Acute bacterial esophagitis is exceedingly rare, particularly in immunocompetent patients. Herein, we describe a unique case of acute streptococcal esophagitis in a male patient with no pertinent medical history. The patient’s substernal chest pain and odynophagia resolved after antibiotic treatment.
Introduction
Infectious esophagitis (IE) is an inflammation of the esophageal mucosa due to infiltration by either a single or multiple microbes. Infectious esophagitis is typically caused by Candida albicans, herpes simplex virus (HSV), and cytomegalovirus (CMV) and is associated with immunosuppression.1-4 Sporadic cases of IE due to Treponema pallidum, human papillomavirus (HPV), varicella-zoster virus, human immunodeficiency virus (HIV), and parasites have also been reported.3-6 Acute bacterial esophagitis is extremely rare, especially in immunocompetent individuals. Bacterial esophagitis is usually due to commensal esophageal bacteria such as Streptococcus species, Staphylococcal species, and Bacillus species.2,5,7,8 Although some patients may be completely asymptomatic, some may present with fever, sore throat, acute dysphagia, odynophagia, retrosternal chest pain, epigastric pain, or weight loss.3,5,9-11 Herein, we report a rare case of acute streptococcal esophagitis in an immunocompetent male patient. The patient presented to our emergency room with acute-onset chest pain and odynophagia. The cardiac workup was unremarkable; however, imaging studies revealed esophageal wall thickening and cervical lymphadenopathy concerning for esophageal neoplasm. The patient was eventually diagnosed with streptococcal esophagitis, which resolved after a course of antibiotics.
Case Summary
A 37-year-old male with a history of alcohol use disorder presented to the emergency department (ED) with acute-onset chest pain. The chest pain was described as substernal, rated as 8/10 in intensity, and radiating to the back. The pain worsened with inspiration, coughing, and movement. Prior to the ED visit, the patient took 2 tablets of ibuprofen 200 mg, which did not alleviate the pain. On review of systems, the patient also endorsed acute odynophagia, especially with solid foods. He denied fever, chills, nasal congestion, recent sick contact, palpitations, shortness of breath, diaphoresis, nausea, vomiting, acid reflux, abdominal pain, recent weight loss, melena, or hematochezia. The patient also denied ingesting any caustic substance, recent steroid use, or a history of esophageal neoplasms or surgery.
In the ED, the patient appeared in acute distress due to chest pain and was unable to sit upright. Vital signs were significant for tachycardia (110 bpm) and elevated blood pressure (151/95 mm Hg). The patient was afebrile and saturated 99% on ambient air. Physical examination revealed positional and pleuritic chest pain. The patient was able to open his mouth appropriately, without any pain. On further inspection of the oral cavity, there was no evidence of angular stomatitis, aphthous ulcers, oral thrush, gingivitis, pharyngitis, stridor, stertor, or pooling of secretions. The rest of the physical examination was similarly non-revealing. Admission blood test results were significant for hyponatremia, hyperkalemia, hyperbilirubinemia, and leukocytosis. Cardiac workup including troponin level and an electrocardiogram (EKG) was unremarkable. Additional tests including HIV, hepatitis panel, urinalysis, pneumonia panel, and viral respiratory panel returned negative (Table 1).
Pertinent Laboratory Findings During the Patient’s Admission.
Computed tomography (CT) angiography of the chest, abdomen, and pelvis ruled out aortic dissection and pulmonary embolism. However, it was significant for mild circumferential thickening of the upper/mid-esophagus with adjacent fat stranding and multiple periesophageal nodes. These findings were concerning for esophageal cancer. The study also revealed the presence of cirrhosis with splenomegaly. A dedicated CT scan of the neck soft tissue with contrast revealed marked wall thickening of the thoracic esophagus with induration of the mediastinal fat and numerous mediastinal lymph nodes and an enlarged right paratracheal node. Similarly, the findings were concerning for esophageal neoplasm vs esophagitis. The CT scan also showed tonsillitis and cervical lymphadenopathy.
Both the antistreptolysin O titer (ASO Ab, 2519.8 IU/mL) and anti-DNase B streptococcal antibodies (Anti-DNase B Strep Abs) were elevated, raising concerns for a recent streptococcal infection. The sputum culture grew few gram-negative rods and gram-positive cocci in chains, consistent with Streptococcus pyogenes. The procalcitonin level was elevated at 3.41 ng/mL. An esophagram showed no fixed obstruction or extraluminal contrast. Esophagogastroduodenoscopy (EGD) revealed small esophageal varices with no stigmata of recent bleeding and a diminutive gastric body polyp (Figure 1). No ulcers, plaques, mucosal friability, or pseudomembranes were noted. The histopathology of the distal and proximal esophagus was significant for focal mild chronic inflammation. Dedicated abdominal ultrasound confirmed cirrhosis and splenomegaly, and the patient was started on carvedilol (6.25 mg, twice daily) as prophylaxis against variceal bleeding.
Endoscopic images showing small, non-bleeding esophageal varices and normal gastric mucosa.
The patient received symptomatic management for odynophagia with phenol 1.4% topical spray and piperacillin-tazobactam. Given the elevated ASO antibodies and anti-DNase B positivity, the patient was diagnosed with acute streptococcal esophagitis and tonsillitis. Immunostaining for Candida, CMV, and HSV-1 and HSV-2 yielded negative results. The patient was successfully treated with a 3-day course of ampicillin-sulbactam (3000 mg, every 6 hours) and discharged with a 4-day course of amoxicillin-clavulanate (875 mg-125 mg, twice daily). The patient was seen in the outpatient clinic 2 weeks after discharge and had no acute complaints.
Discussion
The IE is the second most common cause of esophagitis, second only to gastroesophageal reflux disease.3,4 A higher burden has been observed in immunocompromised hosts due to cancer, cancer-directed therapy, HIV disease, and stem cell or solid organ transplantation.1-4,12 Other risk factors include chronic steroid therapy and uncontrolled diabetes mellitus. 7 Similarly, the indiscriminate use of antibiotics can alter the host microbiome predisposing them to IE. 4 The most common causes of IE are HSV, CMV, and Candida albicans. Bacterial esophagitis is very rare and often a diagnostic enigma. Its low prevalence could, in part, be due to lack of a clear diagnostic criteria or lack of physician awareness. 13 Bacterial esophagitis is typically due to commensal bacteria such as Streptococcal species, Staphylococcal species, Lactobacillus acidophilus, Bacillus species, Corynebacterium species, Actinomycosis, and Nocardia species.2,3,5,7,8,11 Esophageal mucosal injury due to acid reflux, stricture formation, ulceration, or dysmotility creates a nidus for bacterial invasion leading to bacterial esophagitis.5,7-9,14 Herein, we describe a unique case of acute streptococcal esophagitis in a male patient with no pertinent medical history.
Bacterial esophagitis can manifest as sore throat, nausea, vomiting, acute dysphagia, or retrosternal chest pain.3,5,9,10 Esophageal ulcers, persistent heartburn, and hematemesis have also been reported.3,9 As the disease progresses and causes further damage to the mucosa, strictures and stenosis may form causing dysmotility and odynophagia.2,5,7 Further damage to the esophagus may lead to a tracheoesophageal fistula, which can present as dyspnea, recurrent pneumonia, pleural effusions, or pneumothorax. 12 In severe cases, bacterial esophagitis can progress to acute esophageal necrosis and bacteremia, leading to death.9,12
Bacterial esophagitis often presents in a similar fashion as fungal or viral esophagitis. Thus, diagnostic tests, imaging studies, and endoscopic biopsies are vital for an accurate diagnosis. Triage blood tests may reveal leukocytosis or leukopenia depending on the patient’s immune status. Acute blood loss anemia may occur in patients with gastrointestinal bleeding. Positive rapid strep tests and nasal smear cultures may indicate the presence of streptococcal bacteria; however, they do not confirm esophagitis. 2 Esophageal brushings can provide an accurate picture of the microbes present in the esophagus. The absence of hyphae, inclusion bodies, or giant cells in biopsies helps differentiate bacterial esophagitis from other potential causes of IE. 14 Distinguishing bacterial colonization from an active infection remains a challenge. 7 Most cases of streptococcal esophagitis present with non-specific endoscopic findings, such as linear ulcerations, erythema, edema, erosions, mucosal friability, and plaques.2,5,8,9 In addition, endoscopy may reveal other complications, including strictures, stenosis, fistulas, and necrosis.2,12 In mild cases of bacterial esophagitis, EGD findings may be benign. 5 Although our patient’s blood tests and imaging findings were consistent with streptococcal esophagitis, no erythema, ulcers, plaques, or strictures were noted on EGD.
Endoscopic biopsies are critical for differentiating between the different types of esophagitis. In 1984, researchers at The Johns Hopkins Hospital pathology unit identified 23 cases of bacterial esophagitis after examining their oncology patient census. 9 Bacterial esophagitis was described as bacterial colonies on the esophageal mucosa or deeper layers on histopathology, with no evidence of concomitant fungal, viral, or neoplastic involvement or previous esophageal surgeries.2,5,9,14 This case definition was later known as the Walsh criteria for diagnosing bacterial esophagitis. These stringent criteria may have contributed to the low prevalence of bacterial esophagitis cases in the literature. Endoscopic bacterial cultures are not routinely performed in clinical practice because of the high risk of contamination and rarity of bacterial esophagitis.5,9,13,14 As hematoxylin and eosin staining is inadequate for observing bacterial colonies, some cases of bacterial esophagitis can be missed on routine biopsies. Our patient did not meet the Walsh criteria, but his clinical presentation, imaging findings, streptococcal antibody titers, and response to treatment were consistent with streptococcal esophagitis.
The treatment of bacterial esophagitis is largely determined by the presenting symptoms and any potential complications that may arise. As patients may present with bacteremia and sepsis, immediate treatment with intravenous fluids and broad-spectrum antibiotics must be initiated, pending further investigations.9,13,14 Shin et al 2 recommend using beta-lactam antibiotics in combination with a broad-spectrum aminoglycoside for optimal coverage. Once the culture, brushings, and biopsy results return, the treatment regimen can be tailored to the identified organism. Considerations should be made to temporarily decrease any immunosuppressive medications until the infection has been cleared. 7 Proton pump inhibitors may provide symptomatic relief as well as act as a protective agent to prevent further damage to the esophagus, progression of ulcers, and possible bacterial invasions in the future. Relook endoscopy can be performed in patients with persistent symptoms despite treatment for IE. 7 In some cases, bacterial esophagitis can be complicated by ulcers, strictures, and stenosis, warranting more invasive endoscopic interventions. Balloon dilation is the mainstay of treatment for strictures and esophageal stenosis. 2 Patients with acute esophageal necrosis or tracheoesophageal fistulas require surgical intervention. 12
Conclusion
Here, we describe a unique case of acute bacterial esophagitis due to streptococcal pyogenes in a male patient with no pertinent medical history. The patient presented to our ED complaining of acute-onset chest pain and odynophagia. Although the cardiac workup was unremarkable, imaging studies showed esophageal wall thickening and cervical lymphadenopathy concerning for esophageal neoplasm versus esophagitis. The patient was eventually diagnosed with bacterial esophagitis based on streptococcal antibody titers, clinical features, and response to treatment. The IE is usually caused HSV, CMV or Candida albicans. Bacterial esophagitis is extremely rare, and only a few cases have been reported to date.
Footnotes
Author Contributions
N.M. conceptualized the idea of this case report. L.B., D.M., M.F.A., and A.F. helped with data curation, collection of pertinent patient data, and writing of the manuscript. Y.C. and W.B. edited, fact-checked, and proofread the final version of the case report.
Data availability
Further inquiries can be directed to the corresponding author.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
Ethics Approval
Our institution does not require ethical approval for reporting individual cases or case series.
Informed Consent
Verbal informed consent was obtained from the patient for his anonymized information to be published in this article.
