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Related Concept Videos

Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Staphylococcal Skin Infections01:29

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
Streptococcal Pharyngitis01:27

Streptococcal Pharyngitis

Streptococcal pharyngitis, commonly known as “strep throat,” is an acute infection of the oropharyngeal tissues caused by the Gram‑positive Group A Streptococcus (Streptococcus pyogenes). Transmission occurs primarily through respiratory droplets expelled during coughing, sneezing, or talking.Mechanisms of Host Entry and Immune EvasionUpon entering the host, S. pyogenes adheres to the mucosal epithelial cells of the pharynx via surface proteins, notably lipoteichoic acid and the antiphagocytic...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
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Streptococcus bovis causing perforating corneal ulcer.

Atul Jain1, Rajen U Desai, Ruby Jain

  • 1Department of Ophthalmology, Stanford University School of Medicine, Stanford, CA 94304, USA. atuljain@stanford.edu

Cornea
|December 19, 2008
PubMed
Summary
This summary is machine-generated.

This case report details Streptococcus bovis (S. bovis) causing a severe corneal ulcer in a healthy adult. Prompt treatment with vancomycin and ceftriaxone led to a successful corneal transplant.

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Area of Science:

  • Ophthalmology
  • Infectious Diseases

Background:

  • Streptococcus bovis (S. bovis) is a rare cause of ocular infections.
  • Corneal ulcers can rapidly progress and lead to vision loss.

Observation:

  • A healthy 77-year-old male presented with a rapidly progressing corneal ulcer.
  • The ulcer perforated within 4 days of symptom onset.

Findings:

  • Cultures identified S. bovis as the causative agent.
  • The bacteria were susceptible only to vancomycin and ceftriaxone.
  • Histopathology confirmed full-thickness corneal necrosis with bacterial presence.

Implications:

  • This case highlights S. bovis as a potential pathogen in severe corneal ulcers.
  • Early consideration of S. bovis is crucial for appropriate and timely management of rapidly progressing corneal ulcers.