Endogenous endophthalmitis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]
Overview
Endogenous endophthalmitis (EE) also termed metastatic endophthalmitis, is caused by the hematologic dissemination of bacterial or fungal infection to the eyes. Most common extraocular foci of infection include liver abscess, pneumonia, endocarditis, and soft tissue infection. Endogenous endophthalmitis is less common than exogenous endophthalmitis and has been reported to account for 2–8%.
Historical Perspective
Classification
endogenous enophthalmitis may be classified according to causative organisms into 2 subtypes: bacterial or fungal.
Pathophysiology
Pathogenesis
Endogenous endophthalmitis is caused by the hematologic dissemination of an infection to the eyes. Most common extraocular foci of infection include liver abscess, pneumonia, endocarditis, and soft tissue infection. Endogenous endophthalmitis is commonly associated with immunosuppression or procedures that increase the risk for blood-borne infections, such as diabetes, HIV, malignancy, intravenous drug use, transplantation, immunosuppressive therapy, and catheterization. Under normal circumstances, the blood-ocular barrier provides a natural resistance against invading organisms. Following bacteremia, the blood-borne organisms permeate the blood-ocular barrier by:[1][2][3]
- Direct invasion (septic emboli reaches the eye through the posterior segment vasculature)
- Change in vascular endothelium (caused by inflammatory mediators released during infection)
Direct spread from contagious sites can also occur in cases of central nervous system (CNS) infection via the optic nerve.
The exact pathogenesis of candida endophthalmitis is not fully understood. It is though endogenous candida endophthalmitis is commonly associated with abdominal surgery or diabetes mellitus. It is thought immunosuppression alone does not increase the risk of fungemia and subsequent fungal endophthalmitis.
The asexual spores of aspergilli organisms are airborne. Following inhalation of an airborne organism into the body, the aspergilli spores enter the terminal alveoli of the lung. Under normal circumstances, the lung provides a natural resistance against invading organisms. But in high risk patients, such as those patients with history of chronic pulmonary diseases], history of organ transplant, intravenous drug abuse, cardiac surgery, and alcoholism, disseminated aspergillosis may result in endogenous endophthalmitis.
Gross Pathology
On gross pathology, eyelid swelling, eyelid erythema, conjunctival injection, chemosis, and mucoprulunt dischage are characteristic findings of endogenous endophthalmitis.
Microscopic histopathological analysis
- On microscopic histopathological analysis, infiltration of polymorphonuclear leukocytes and destruction of ocular structures are characteristic findings of endogeouse bacterial endophthalmitis.
- On microscopic histopathological analysis, random vitreouse and retinal lesions with polymorphonoclear leukocytes, lymphocytes, budding yeast, pseudohyphae, and choroidal/retinal wall invasion are characteristic findings of candida endophthalmitis.
- On microscopic histopathological analysis, angiocentric retinal and choroidal lesion, mixed acute and chronic inflammatory cells infiltration, retinal and choroidal vessel invassion, subretinal pigment epithelial and subretinal infection are characteristic findings of aspergillus endophthalmitis.[4] [5]
Causes
Common causes of endogenous endophthalmitis include:[1][2][3]
Bacterial
- Gram-positive bacteria
- Streptococcus pneumoniae
- Staphylococcus aureus
- Bacillus cereus (primary bacterial cause in intravenous drug abusers)
- Gram-negative bacteria
- Neisseria meningitidis (pre-antibiotic era)
- Escherichia coli
- Klebsiella (in the Asian population with liver abscess)
Fungal
Differentiating endogenous Endophthalmitis from Other Diseases
- Cytomegalvirus retinitis
- Toxoplasmosis retinochoroiditis
- Coccidiomycosis choroiditis
- Bacterial endophthalmaitis
Epidemiology and Demographics
Risk Factors
Endogenous bacterial endophthalmitis
Common risk factors in the development of endogenous bacterial endophthalmitis include:[1][2][3]
- Recent hospitalization
- Immunosuppression
- Diabetes mellitus
- Urinary tract infection
- Immunosuppression (associated with underlying malignancy, neutropenia, and HIV)
- Intravenous drug use
- Catheterization
- Long-term use of broad-spectrum antibiotics or immunosuppressive drugs
- Liver abscess
- [Infective endocarditis (IE)
Endogenous fungal endophthalmitis
Common risk factors in the development of endogenous fungal endophthalmitis include:
- Chemotherapy
- Organ transplantation (cardiac and liver transplants)
- Immunosuppressive therapy for hematopoietic stem cell transplantation (HSCT)
- Lung involvement by Aspergillus
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
X Ray
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ 1.0 1.1 1.2 Durand ML (2013). "Endophthalmitis". Clin Microbiol Infect. 19 (3): 227–34. doi:10.1111/1469-0691.12118. PMC 3638360. PMID 23438028.
- ↑ 2.0 2.1 2.2 Kernt M, Kampik A (2010). "Endophthalmitis: Pathogenesis, clinical presentation, management, and perspectives". Clin Ophthalmol. 4: 121–35. PMC 2850824. PMID 20390032.
- ↑ 3.0 3.1 3.2 Wong JS, Chan TK, Lee HM, Chee SP (2000). "Endogenous bacterial endophthalmitis: an east Asian experience and a reappraisal of a severe ocular affliction". Ophthalmology. 107 (8): 1483–91. PMID 10919895.
- ↑ Rao, Narsing A., and Ahmed A. Hidayat. "Endogenous mycotic endophthalmitis: variations in clinical and histopathologic changes in candidiasis compared with aspergillosis." American journal of ophthalmology 132.2 (2001): 244-251.
- ↑ Hunt, LCDR Kerry E., and Ben J. Glasgow. "Aspergillus endophthalmitis: an unrecognized endemic disease in orthotopic liver transplantation." Ophthalmology 103.5 (1996): 757-767.