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Incidence and Risk Factors of Bilateral Herpetic Keratitis: History
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Contributor: Stergios Konstantinos Chaloulis , George Epameinondas Mousteris , Konstantinos Tsaousis

Herpetic keratitis is the result of a corneal infection with Herpes Simplex Virus (HSV) and it is recognized as a leading cause of corneal blindness worldwide. Bilateral HSV keratitis is a rare clinical manifestation and consists of simultaneously occurring infection in both eyes.

  • Herpes Simplex Virus
  • bilateral herpetic keratitis
  • disciform keratitis

1. Introduction

The term “herpes” is derived from the Greek word “herpein” [pronounced: érpin], which means “creeping or crawling” and stands for the characteristic creeping of the eruptions caused by the virus [1].
Herpes Simplex Virus is a linear double-stranded DNA virus that is an Alpha-herpesvirinae member of the Herpesviridae family. Common pathogens in the Herpes family are Herpes Simplex Viruses 1 and 2 (HSV-1 and HSV-2), Varicella-Zoster Virus (VZV). Another common pathogen (member of Gamma herpes virus family) is Epstein–Barr Virus (EBV). All the above-mentioned viruses are neurotrophic, meaning that they have the ability to reside in a latent state within neurons of the sensory and autonomic ganglia from where they can reactivate occasionally, making the host a lifetime carrier [2].
While Herpes Simplex Virus (HSV) can infect any part of the body and elicit a variety of serious diseases in humans, it commonly infects the face, genitals and eyes with skin/face infections, typically a consequence of either oral or ocular infection [2][3]. The virus is most commonly transmitted by droplets of infected secretions, such as tears and saliva, or by direct contact of skin sores [3][4][5][6]. It was previously thought that HSV-1 had a predilection for the trigeminal ganglion and HSV-2 for the sacral ganglion [4][6]. However, ocular infection can be caused by both HSV-1 and HSV-2 [1][3]. Corneal infection is due to direct inoculation. HSV-1 may be spread to the eyes from facial sores or secretions, while HSV-2 may get transmitted either venereally, or at birth during the passage of the neonate through the vaginal tube. Conditions of crowding and poor hygiene may also facilitate transmission [5].
Primary ocular HSV infection is usually asymptomatic depending on immunological status of the host [7]. Corneal epithelial cells express specific receptors (Nectin 1, HVEM and PILR-alpha, etc.) that facilitate viral entry into the cells [5]. On contact, the virus enters the epithelial cells and starts replicating. Within hours, it enters the sensory nerve, which innervates the initial site of infection, and travels to the sensory ganglion (the trigeminal ganglion), where it may remain in a dormant state, called latency. Alternatively, it may replicate and travel back along the nerve to cause a primary infection that is clinically evident in 1% to 6% of infected patients. It can manifest as conjunctivitis, blepharitis, lid ulcers and vesicles with corneal signs seen in 33% patients. It often goes undiagnosed, especially when symptoms are mild [4][7].
Once the primary infection resolves, the virus becomes latent and stores its genome in the nucleus of a host cell, unlike retroviruses, which integrate their genome into the host’s DNA. During its latency, HSV-1 produces latency-associated transcripts (LATs) that maintain the integrity of the viral genome and reduce cellular apoptosis [8]. Later, at any point in life, certain triggers promote HSV to reactivate. The virus then utilizes the host cell’s DNA polymerase to transcribe and replicate [9], and finally it travels back down the nerve to cause a recurrent infection [4][7]. Weakening of the immune system and the presence of inflammatory mediators, such as cytokines, play an important role in the reactivation of HSV [10].
Recrudescent HSV infections are usually due to reactivation of the HSV strain acquired during primary infection. However, superinfection with a new HSV strain at the site of primary infection has also been documented [2].

2. Epidemiology

HSV-1 and -2 infect up to 90% of adults in the world. HSV-1 alone infects 66% of the world’s population. However, in some developing parts of the world, such as Latin America and sub-Saharan Africa, the prevalence of HSV-1 surpasses 90% [8].
Bilateral herpetic keratitis reported incidence in literature varies from 1.3% to 12% depending on the criteria used to diagnose it [7][9]. A 30-year retrospective study in the U.S. estimated the annual incidence of ocular HSV at 11.8 new cases per 100,000 of population. According to that study, 4% of all patients identified with HSV keratitis had simultaneous, bilateral involvement at initial presentation, and an additional 1% developed simultaneous bilateral involvement at the time of recurrence. Annual rates were similar between men and women. In addition, an increasing rate was recorded with aging [11]. Another large Korean study reported a 12% rate of bilateral disease among all HSV keratitis cases [12]. A study conducted in India reported a notably higher incidence of bilateral HSV keratitis, up to 25% of all herpetic keratitis cases [13]. Higher bilateral rates have also been reported in pediatric patients [14] and in patients with immunosuppression or other underlying conditions [15][16]. Table 1 summarizes the incidence rates reported in literature.
Table 1. Incidence of bilateral HSV keratitis in previous studies.
Study Setting Incidence of Bilateral HSV Eye Cases Description of Bilateral HSV Keratitis Cases
Ref. [12] Clinical Features of Herpes Simplex keratitis in a Korean Tertiary Referral center. Efficacy of Oral Antiviral and Ascorbic Acid on Recurrence Retrospective study from January 2010 to January 2015 at Gyeongsang National University Hospital in Jinju, South Korea 16/133 patients
12.0%		 The patients were followed for 24.1 + −13.2 months on average
The mean age of onset was 61.1 + −15.6 years
The mean BCVA at onset was 0.65 + −0.63
Ref. [17] Ocular involvement and visual outcome of Herpes Zoster ofthalmicus: review of 45 patients from Tunisia, North Africa Retrospective study from January 2000 to January 2012
Department of Ofthalmology at Fattouma Bourguiba Hospital of Monastir, Tunisia		 6 of 45 patients
13.3%		 2 of them had diabetes
2 were under immunosuppressive therapy
1 had HIV infection and the past medical history was remarkable in the remaining 1 patient
Ref. [11] The Incidence, Recurrence and Outcomes of Herpes Simplex Virus Eyes Disease in Olmsted County, Minnesota, 1976 through 2007: the impact of Oral Antiviral Prophylaxis Retrospective study from 1976 to 2007 at Olmsted County, Minnesota 20 of 394 patients
5%		 16 of them had bilateral involvement at initial presentation
4 additional patients had bilateral involvement at the time of recurrence
Ref. [2] Corneal Herpes Simplex Virus Type I Superinfection in patients with Recrudescent Herpetic Keratitis Rotterdam Eye Hospital, Rotterdam The Netherlands 1 of 30 patients 3.33% In this patient the bilateral herpetic keratitis was due to infections with different HSV-1 strains in either cornea
Ref. [13] Clinical profile of Herpes Simplex Keratitis cases attending eye Opd in tertiary hospital Chhattisgarh state Prospective study from March 2016 to February 2017 at the Department of ophthalmology, Government Medical College, Rajnandgaon, India 20 of 80 patients 25% In a series of 356 patients over 30 years in Japan bilateral keratitis was found in 9.4%. This may be due to overall increased incidence of the disease.
Bilateral cases are mainly epithelial keratitis which complies with other study.
Ref. [15] Bilateral Herpetic Keratocunjunctivitis in cancer patients Retrospective study from June 2001 to August 2011 at MD Anderson Cancer Center 12 of 90 patients 13.3% 5 of them were in remission from their cancer and the other 7 were in active cancer treatment
Only 2 patients were not immunocompromised or suppressed
7 of the patients were on systemic steroids and the other 5 were on prophylactic anti-viral medication at the time of presentation.
1 of them had disseminated herpetic disease and was on IV antiviral therapy
Ref. [16] Herpes Simplex Keratitis in Rheumatoid Arthritis Patients Retrospective study 2 of 5 patients 40%  
Ref. [14] Herpes simplex virus keratitis in children Retrospective cohort study 6 of 23 patients 26%  
Ref. [18] Bilateral herpetic keratoconjunctivitis Retrospective study from January 1996 to September 2001 at the Department of Opthalmology, University of Minnesota 7 of 544 patients 1.3% 5 of these patients had systemic atopy and the other 2 ocular rosacea
Systemic immune disorders were noted in two patients.
Recurrent blepharoconjunctivitis was noted in 8 eyes (57%),
epithelial keratitis in 12 eyes (85.7%)
stromal keratitis in 9 eyes (64.3%) necrotizing stromal keratitis in 5 eyes (35.7%)
progressive endotheliitis in 2 eyes (14.2%).
Penetrating keratoplasty was performed in 1 eye, in which endophthalmitis subsequently developed and which required enucleation.

3. Clinical Presentation

HSV can affect all layers of the cornea. Depending on the clinical features identified on slit-lamp examination, herpetic keratitis is characterized as: Epithelial keratitis, immune or necrotizing stromal keratitis, neurotrophic keratopathy and endotheliitis, according to a recent renewal of the classification of HSK [1].
Common symptoms include redness, discharge, watery eyes, irritation, itching or foreign body sensation, and photophobia. In most patients, symptoms begin to subside after the first 2 weeks [9].
The most common subtype, epithelial keratitis, is usually due to an actively replicating virus and appears as coarse granular spots that form punctate or stellate lesions, but these quickly coalesce to form dendritic lesions. On the slit-lamp examination, epithelial keratitis presents as a dendritic lesion with terminal buds, swollen borders and intraepithelial cell infiltration. The ulcer may progressively increase in size to give a “geographical” or “amoeboid” configuration [3][5][9], especially in patients with local or systemic immunosuppression.
Stromal keratitis on physical examination appears opaque or whitened, due to stromal infiltration. Descemet membrane folds might be present as well. Corneal sensation is often reduced [13]. Similarly, the necrotizing form appears as gray-white or opaque, but there is accompanying necrosis and ulceration on slit-lamp examination. Edema and abscess may be apparent as well [3][9]. It can often result to perforation [13].
Another form of HSK, disciform lesion, has a ground-glass appearance and is disk-shaped with stromal edema (alike to different forms of endothelial keratitis) on slit-lamp examination. Neurotrophic ulcer appears with persistent central epithelial defects with a grey thickened border (Wessely immune ring) [5]. Lastly, the endothelial form appears with medium-sized keratic precipitates. Aqueous flare and cells and iritis may be visible. Stromal edema is also present [3][9][13].
Intraocular pressure could be elevated [5] when the infection causes trabecular meshwork inflammation. Bilateral herpetic keratitis presenting as peripheral ulcerative keratitis (PUK) is an extremely rare manifestation of herpetic disease. PUK can pose a diagnostic dilemma in cases with immune system disorders, such as rheumatoid arthritis. Excluding infectious agents is mandatory for appropriate treatment [16][19][20].

4. Diagnostic Procedures

Herpes Simplex is usually diagnosed clinically and requires no laboratory confirmation. If the diagnosis is in doubt, the following tests may assist: [5][9][21]
  • Polymerase chain reaction (PCR).
  • Scrapings of corneal or skin lesions for Giemsa stain or Tzanck smear—ELISA testing.
  • Viral culture.
  • HSV antibody titers. They rise after primary but not recurrent infection.
Immunofluorescence antibody assay (IFA) of tears.
PCR is highly sensitive, but large variation has been observed in numerous studies between the rates of HSV detection by PCR when compared to clinical diagnosis. PCR diagnostic effectiveness may be affected in patients under prophylactic anti-viral treatment with acyclovir. In addition, topical anesthetics and dyes, such as fluorescein, Bengal rose and lissamine green used for clinical diagnosis of HSV may result in decreased sensitivity of the PCR assay. The type of specimen used in detection of HSV with PCR is also an important factor. Tear specimen produces significantly less sensitive results than corneal scrapings [9]. PCR and in situ hybridization are effective and powerful techniques when other virological procedures are non-contributive, particularly in immunocompromised patients previously treated with antiviral drugs [22].

5. Differential Diagnosis

Misdiagnosis in clinical settings is not uncommon. Simultaneously bilateral corneal lesions resembling herpetic keratitis can be due to multiple causes such as infectious keratitis from other pathogens, post-traumatic corneal erosions, chemical injury, dystrophies, degenerations and rarely acute hydrops. Sterile corneal melt resulting from multiple eye conditions such as dry eyes, connective tissue disorder and nutritional deficiency can also result in involvement of both eyes at the same time [7][9].
Literature underscores that a significant percentage of the clinically diagnosed bilateral HSV lesions were actually caused by Varicella-Zoster Virus, adenovirus, Cytomegalovirus or Enterovirus, as confirmed by laboratory tests [9].

6. Risk Factors

6.1. Systemic Diseases—Immunodeficiency Conditions

Rheumatoid arthritis (RA) is an autoimmune disease, characterized by an irregular immune response towards components of the connective tissue, such as collagen and elastin, also present in the structure of the cornea, and it is associated with higher incidence of bilateral HSV keratitis (40%). The characteristics of HSK in patients with RA differ from HSK in immunocompetent patients. Stromal keratitis cases were very aggressive and difficult to manage, with perforation and Gram-positive bacterial co-infection as frequently associated conditions. Prophylactic therapy at standard doses has proven unsuccessful to prevent recurrences [16]. These patients of course are usually under anti-inflammatory/immunosuppressive treatment that also favors the reactivation of HSV.
Human Immunodeficiency Virus (HIV) infection results in many cases in acquired immunodeficiency syndrome (AIDS), which is characterized by depletion of CD4+ white blood cells. A 10-year retrospective study in Tunisia reported the ocular disorders related to the disease in people living with HIV (PLWH). Most patients (86%) were on ART (Tenofovir + emtricitabine + efavirenz) combination therapy. Immunodeficiency caused by the virus increased susceptibility to opportunistic infections and neoplasms. Herpes Simplex Keratitis was found in 5% of those patients. The risk of developing ocular disease in PLWH is higher when the CD4+ count is <200 cells/μL [21].
Another category of immunocompromised patients is organ transplant recipients, as they are under long-term treatment with immunosuppressive drugs to prevent graft rejection—failure.
Cancer patients are also prone to develop bilateral herpetic keratitis. A 10-year review studied patients with malignancies that developed herpes simplex or zoster keratoconjunctivitis; 13.3% of them had bilateral disease. For the bilateral cases, the cancer diagnoses included leukemia, lymphoma/myeloma, breast and colon cancer. Only 16% of the patients were not immunocompromised or suppressed (receiving only X-ray treatment), but all others were either being actively treated for their relapsed cancer (with chemo/steroids) or immunosuppression after allogeneic stem cell transplantation (SCT) [15].

6.2. Age

6.2.1. Childhood

There are several studies highlighting that HSV keratitis occurs more frequently as bilateral disease in the pediatric population [7][14][23][24]. The most common clinical manifestations are epithelial dendritic keratitis (38.5%) and interstitial keratitis (35.7%) [23]. Although the clinical appearance of ocular Herpes Simplex Virus (HSV) is similar in children and adults, there is evidence that stromal disease and recurrences are present in higher rates among pediatric patients [14][23][25]. Misdiagnosis of these patients is common, and therefore they are at higher risk to develop corneal scarring and opacity ultimately leading to amblyopia [14][25].
A Nigerian study in children with keratitis reported that approximately 79% of patients with HSV had combined epithelial and stromal disease. Keratitis was associated with a recent measles infection and protein calorie malnutrition. Bilateral HSV was recorded in 12.7% among herpetic cases [24].

6.2.2. Senility

Increased age has been associated with reduced cell-mediated immunity, which is a crucial factor to avoid reactivation of latent viral infections, such as herpes zoster [17].
A large 30-year retrospective study in Minnesota found an age-related increased incidence in new cases of HSV keratitis, suggesting similarly the decreased immunity in elderly people as the possible cause [11].

6.3. Medications

Various immunosuppressive drugs have been linked to the reactivation of viral infections.
Corticosteroids are widely used as systemic treatment in a plethora of indications, including autoimmune diseases and atopy, to mitigate the immune system’s response and reduce inflammation. A latent HSV infection could be reactivated by rapid tapering of systemic corticosteroids, as both steroid use and rapid tapering may act as a triggering factor for viral infection or reactivation of herpes [26].
Rituximab is a B cell depleting anti-CD20 monoclonal antibody that is increasingly used to treat autoimmune disorders and B cell non-Hodgkins lymphoma. As with other immunosuppressive agents, there is the risk of opportunistic infections or reactivations, including Hepatitis-B virus and Herpes viruses (HSV). There is a rare case report of a patient suffering from severe mucous membrane pemphigoid treated with rituximab who developed herpetic keratitis. A 71-year-old patient suffered from severe mucous membrane pemphigoid (an autoimmune blistering disease affecting predominantly the mucosae) with ocular, oral pharyngeal and laryngeal involvement. To control the disease, the patient was given rituximab therapy in combination with oral corticosteroids. He subsequently experienced an epithelial herpes simplex virus keratitis in one eye and 3 months later in his other eye [27].
Ocular anti-hypertension drugs and prostaglandin analogs. There is a strong debate in literature about the role of anti-glaucoma drugs and prostaglandin analogs, especially in triggering recurrent herpetic keratitis.
Several case reports suggested a causal relationship between the use of topical prostaglandin eye drops and episodes of bilateral HSV keratitis. Both latanoprost [28], travoprost [3] and bimatoprost [29][30] were thought accountable. Authors support their hypothesis with the observation that all incidents happened during the use of anti-glaucoma drops and that the patients had no other predisposing factors to explain recurrence of keratitis [2]. Moreover, by administrating anti-viral agents patients recovered within days [29] and by discontinuing the suspected drug there were no recurrences of keratitis [28]. Additionally, in some cases, when the patient resumed treatment with the same drug, bilateral keratitis re-occurred [3][29] with increased severity [30]. Antiglaucoma prostaglandin analogues induce the release of endogenous prostaglandins in the iris and the ciliary muscle, acting as inflammation mediators. This mechanism probably explains the reactivation of HSV keratitis [29]. All these reports share a common weakness: Diagnosis of HSV relied on clinical findings only, without laboratory confirmation.
Some authors, however, acknowledge that corneal toxicity from the preservative contained in eye drops may have contributed to herpes’ reactivation [3]. In addition, a recent case series study emphasizes that corneal toxicity is commonly misdiagnosed by physicians as herpetic keratitis, due to the similar appearance of corneal lesions. The study included patients under treatment with all categories of anti-glaucoma drops, initially referred with presumed diagnosis of HSK. Half of them had bilateral corneal lesions. Most drops in the study also contained benzalkonium (BAK) as a preservative. Daily and repetitive exposure of ocular surface to the active compounds and the preservatives in the topical anti-glaucoma medications is often reported to cause toxic effects to the ocular surface. Furthermore, both HSK and chronic use of topical medications containing BAK can cause impaired corneal sensation [31].
Corneal toxicity usually appears as punctate epithelial defects, which over time collide to form linear or branch-like lesions resembling the characteristic herpetic dendritic lesions. The main distinctive details are that the pseudodendritic lesions have rather heaped-up edges, they lack terminal buds and they are usually surrounded by diffuse punctate defects. The authors using specific clinical criteria determined that their patients’ lesions were not actually related to HSV and confirmed their findings with negative viral cultures. All patients recovered after removal of the presumed triggering medication or by applying ocular surface protecting methods, including topical lubricants or therapeutic soft contact lens, and without the need of anti-viral treatment [31].

This entry is adapted from the peer-reviewed paper 10.3390/tropicalmed7060092

References

  1. Hamrah, P.; Pavan-Langston, D.; Dana, R. Herpes Simplex Keratitis and Dendritic Cells at the Crossroads. Int. Ophthalmol. Clin. 2009, 49, 53–62.
  2. Remeijer, L.; Maertzdorf, J.; Buitenwerf, J.; Osterhaus, A.D.M.E.; Verjans, G.M.G.M. Corneal Herpes Simplex Virus Type 1 Superinfection in Patients with Recrudescent Herpetic Keratitis. Investig. Ophthalmol. Vis. Sci. 2002, 43, 358–363.
  3. Zwerling, C.-S.; Naithani, R. Bilateral Herpes Simplex Keratitis Presenting as Bilateral Ulcerative Blepharo-Keratoconjunctivitis: A Rarity or Pattern. Ann. Rev. Res. 2021, 6, 555683.
  4. Aggarwal, S.; Pawaiya, S.; Kenguva, S.; Bhardwaj, A.; Saxena, H. Bilateral Disciform Keratitis: A Rare Entity. Santosh Univ. J. Health Sci. 2019, 5, 48–49.
  5. Ahmad, B.; Patel, B.C. Herpes Simplex Keratitis. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022.
  6. Kaye, S. Herpes Simplex Keratitis: Bilateral Effects. Investig. Ophthalmol. Vis. Sci. 2015, 56, 4907.
  7. Agarwal, R.; Maharana, P.K.; Titiyal, J.S.; Sharma, N. Bilateral Herpes Simplex Keratitis: Lactation a Trigger for Recurrence! BMJ Case Rep. 2019, 12, e223713.
  8. Koganti, R.; Yadavalli, T.; Shukla, D. Current and Emerging Therapies for Ocular Herpes Simplex Virus Type-1 Infections. Microorganisms 2019, 7, 429.
  9. Azher, T.N.; Yin, X.-T.; Tajfirouz, D.; Huang, A.J.; Stuart, P.M. Herpes Simplex Keratitis: Challenges in Diagnosis and Clinical Management. Clin. Ophthalmol. 2017, 11, 185–191.
  10. Majtanova, N.; Kriskova, P.; Keri, P.; Fellner, Z.; Majtan, J.; Kolar, P. Herpes Simplex Keratitis in Patients with SARS-CoV-2 Infection: A Series of Five Cases. Medicina 2021, 57, 412.
  11. Young, R.C.; Hodge, D.O.; Liesegang, T.J.; Baratz, K.H. Incidence, Recurrence, and Outcomes of Herpes Simplex Virus Eye Disease in Olmsted County, Minnesota, 1976–2007: The Effect of Oral Antiviral Prophylaxis. Arch. Ophthalmol. 2010, 128, 1178–1183.
  12. Kim, G.N.; Yoo, W.S.; Park, M.H.; Chung, J.K.; Han, Y.S.; Chung, I.Y.; Seo, S.W.; Yoo, J.M.; Kim, S.J. Clinical Features of Herpes Simplex Keratitis in a Korean Tertiary Referral Center: Efficacy of Oral Antiviral and Ascorbic Acid on Recurrence. Korean J. Ophthalmol. 2018, 32, 353–360.
  13. Sinha, A.; Dulani, S. Clinical Profile of Herpes Simplex Viral Keratitis Cases Attending Eye Opd in Tertiary Hospital of Chhattisgarh State. Indian J. Clin. Exp. Ophthalmol. 2021, 3, 440–443.
  14. Chong, E.-M.; Wilhelmus, K.R.; Matoba, A.Y.; Jones, D.B.; Coats, D.K.; Paysse, E.A. Herpes Simplex Virus Keratitis in Children. Am. J. Ophthalmol. 2004, 138, 474–475.
  15. Canseco, E.; Modak, J.; Kingham, A.; Arevalo, V.; Kim, S.K. Bilateral Herpetic Keratoconjunctivitis in Cancer Patients. Investig. Ophthalmol. Vis. Sci. 2012, 53, 6149.
  16. Larrañaga Fragoso, P.; Boto de Los Bueis, A.; Bravo Ljubetic, L.; Del Hierro Zarzuelo, A.; Romero Gómez, M.P.; Mora Rillo, M. Herpes Simplex Keratitis in Rheumatoid Arthritis Patients. Ocul. Immunol. Inflamm. 2016, 24, 282–287.
  17. Kahloun, R.; Attia, S.; Jelliti, B.; Attia, A.Z.; Khochtali, S.; Yahia, S.B.; Zaouali, S.; Khairallah, M. Ocular Involvement and Visual Outcome of Herpes Zoster Ophthalmicus: Review of 45 Patients from Tunisia, North Africa. J. Ophthalmic Inflamm. Infect. 2014, 4, 25.
  18. Souza, P.M.F.; Holland, E.J.; Huang, A.J.W. Bilateral Herpetic Keratoconjunctivitis. Ophthalmology 2003, 110, 493–496.
  19. Chranioti, A.; Malamas, A.; Metallidis, S.; Mataftsi, A.; Chalvatzis, N.; Ziakas, N. Bilateral Herpes Simplex Virus-Related Peripheral Ulcerative Keratitis Leading to Corneal Perforation in a Patient with Primary Herpes Simplex Virus Infection. J. Ophthalmic Vis. Res. 2019, 14, 93–96.
  20. Praidou, A.; Androudi, S.; Kanonidou, E.; Konidaris, V.; Alexandridis, A.; Brazitikos, P. Bilateral Herpes Simplex Keratitis Presenting as Peripheral Ulcerative Keratitis. Cornea 2012, 31, 570–571.
  21. Saadouli, D.; Ammari, L.; Ben Mansour, K.; Yahyaoui, Y.; Aissa, S.; Mohamed Ali, E.A.; Yahyaoui, S.; Tiouri, H. Ocular Manifestations of People Living with HIV in Tunisia. S. Afr. J. HIV Med. 2021, 22, 1193.
  22. Bodaghi, B.; Mougin, C.; Michelson, S.; Agut, H.; Dighiero, P.; Offret, H.; Frau, E. Acyclovir-Resistant Bilateral Keratitis Associated with Mutations in the HSV-1 Thymidine Kinase Gene. Exp. Eye Res. 2000, 71, 353–359.
  23. Serna-Ojeda, J.C.; Ramirez-Miranda, A.; Navas, A.; Jimenez-Corona, A.; Graue-Hernandez, E.O. Herpes Simplex Virus Disease of the Anterior Segment in Children. Cornea 2015, 34 (Suppl. 10), S68–S71.
  24. Ashaye, A.; Aimola, A. Keratitis in Children as Seen in a Tertiary Hospital in Africa. J. Natl. Med. Assoc. 2008, 100, 386–390.
  25. Bodack, M.I. Case Series: Pediatric Herpes Simplex Keratitis. Optom. Vis. Sci. 2019, 96, 221–226.
  26. Yang, H.K.; Han, Y.K.; Wee, W.R.; Lee, J.H.; Kwon, J.W. Bilateral Herpetic Keratitis Presenting with Unilateral Neurotrophic Keratitis in Pemphigus Foliaceus: A Case Report. J. Med. Case Rep. 2011, 5, 328.
  27. Bernauer, W.; Schuler, S.; Borradori, L. Rituximab and Bilateral HSV Epithelial Keratitis in a Patient with Mucous Membrane Pemphigoid. J. Ophthalmic Inflamm. Infect. 2018, 8, 12.
  28. Ekatomatis, P. Herpes Simplex Dendritic Keratitis after Treatment with Latanoprost for Primary Open Angle Glaucoma. Br. J. Ophthalmol. 2001, 85, 1008–1009.
  29. Jdms, I. Bimatoprost and Herpetic Keratitis—A Rare Association. Available online: https://www.academia.edu/36900761/Bimatoprost_and_Herpetic_Keratitis_A_Rare_Association (accessed on 17 January 2022).
  30. Kothari, M.T.; Mehta, B.K.; Asher, N.S.; Kothari, K.J. Recurrence of Bilateral Herpes Simplex Virus Keratitis Following Bimatoprost Use. Indian J. Ophthalmol. 2006, 54, 47–48.
  31. Chang, H.-L.; Kuo, B.-I.; Wu, J.-H.; Huang, W.-L.; Su, C.-C.; Chen, W.-L. Anti-Glaucoma Agents-Induced Pseudodendritic Keratitis Presumed to Be Herpetic Simplex Keratitis: A Clinical Case Series. Sci. Rep. 2021, 11, 21443.
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