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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 21  |  Issue : 1  |  Page : 34-37

Endogenous endophthalmitis caused by Aspergillus flavus in an immunocompetent individual – A rare case with review of literature


Department of Microbiology, Aravind Eye Hospital, Salem, Tamil Nadu, India

Date of Web Publication12-Aug-2019

Correspondence Address:
Dr. Suneetha Viswanathaiah
W/o Dr. Puneeth C S, Flat A, Brindhavan Tamil Apartment, Ezhlil Nagar, Nagarmalai Adivaram Road, Salem - 636 016, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jacm.jacm_8_18

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  Abstract 


There are very few reports of Aspergillus flavus causing endogenous Aspergillus endophthalmitis (EAE) in immunocompetent individuals although it is well recognized in the immunocompromised. Treatment can be with intravitreal, intravenous and oral antifungal agents. We present a case of EAE in a 23-year-old female with no predisposing risk factors. A detailed systemic evaluation failed to reveal any systemic focus or predisposing factor for fungal infection. The patient had received an intravenous dextrose infusion two days before this episode while being treated at a rural hospital for fever. She presented with a sudden loss of vision and was subsequently managed with intravitreal voriconazole therapy. This case adds to the limited literature on the prevalence of endogenous endophthalmitis in immunocompetent patients and supports the use of voriconazole in such cases.

Keywords: Aspergillus flavus, endogenous endophthalmitis, immunocompetent


How to cite this article:
Viswanathaiah S, Babu M, Manjunatha M. Endogenous endophthalmitis caused by Aspergillus flavus in an immunocompetent individual – A rare case with review of literature. J Acad Clin Microbiol 2019;21:34-7

How to cite this URL:
Viswanathaiah S, Babu M, Manjunatha M. Endogenous endophthalmitis caused by Aspergillus flavus in an immunocompetent individual – A rare case with review of literature. J Acad Clin Microbiol [serial online] 2019 [cited 2019 Aug 20];21:34-7. Available from: http://www.jacmjournal.org/text.asp?2019/21/1/34/264254




  Introduction Top


Endophthalmitis is an inflammatory condition of intraocular cavities (aqueous or vitreous humour) usually caused by infection either by bacteria/fungi/viruses/parasites. Non-infective endophthalmitis can also occur sometimes due to irritation caused by retained lens material or some toxic products.

Exogenous endophthalmitis is most common and often seen in penetrating injuries, post-surgical complication or spread of external eye infection.

In contrast, endogenous endophthalmitis (EE) is rare and occurs due to the haematogenous spread of organisms into the eye from a remote primary source. This condition is relatively not common accounting for 6%–7% of all cases of endophthalmitis and is usually associated with immunocompromised state, debilitated diseases and invasive procedures.[1] EE in an immunocompetent individual is very rare.

Many etiologic agents have been reported to cause EE. Both bacterial and fungal agents are noted in the literature as potential agents of EE in the developed world. However, fungal organisms account for the majority of the cases.[2]

Among the different fungi causing EE, Candida is the most common cause of infection followed by Aspergillus species.[3]

Aspergillus is a fungus, usually considered a harmless saprophyte, which is ubiquitous in the environment. Aspergillus infections commonly present as a localized disease of the lungs or paranasal sinuses and mainly affect immunocompromised individuals.

Aspergillus causing EE is rare and is usually associated with disseminated disease among patients with chronic lung disease, cancer, intravenous drug abuse, immunocompromised state or after liver transplantation.[4]

In rare instances, Aspergillus endophthalmitis may occur in immunocompetent patients with no apparent predisposing factors.[5] Aspergillus fumigatus and Aspergillus flavus are the species most frequently isolated from patients with intraocular infection. Since endophthalmitis caused by Aspergillus species presents abruptly and progresses rapidly to irreversible retinal damage, rapid recognition is very important. Early diagnosis and appropriate treatment may increase the likelihood of favourable outcome. Voriconazole is a usual treatment of choice to treat Aspergillus infection.

We reported a rare case of endogenous A. flavus endophthalmitis in a 25-year-old female patient.


  Case Report Top


A 23-year-old female patient presented with a history of sudden loss of vision in the left eye since four days, with mild ocular pain. She had a fever with headache for one week. There was no past history of trauma or any other external eye infection, surgery, malignancy or any other immunocompromised condition. She gave a history of cutaneous lesions on and off for one year, for which she was applying topical steroids. She also received one bottle intravenous infusion of dextrose normal saline in a local hospital two days before the ocular symptoms. On examination, the right eye was normal. There was a reduction in her visual acuity on the left to hand movements only (1/60 unaided). There was a mild congestion of conjunctiva. On slit-lamp examination, the aqueous showed 3+ cells/HPF and 2+ flare. Keratic precipitates present. Intraocular pressure in the left eye was 5 mmHg. Lens was clear. Vitreous was completely hazy. An ultrasound B scan of the left eye showed dot echoes suggestive of vitreous inflammation (vitritis). Clinically, this was suspected to be panuveitis or endophthalmitis. Vitreous trap was done and sent for KOH, Gram stain and culture. Intravitreal 0.1 ml of ceftazidime (2.25 mg), 0.1 ml of vancomycin 1 mg and 0.1 ml of voriconazole (100 μg) were given and started empirically with topical moxifloxacin 0.5%, 1 drop every fourth hourly and voriconazole 1% eye drop, 1 drop every ½ hourly. The Gram stain of the vitreous biopsy showed a moderate number of polymorphonuclear cells, branching septate hyphae and no bacteria. Bacterial cultures were negative but the culture on potato dextrose agar revealed a mould identified as A. flavus. This was identified on the basis of typical colonial and microscopic morphologies. Core vitrectomy was done after two days. Anterior chamber wash was done and exudates cleared. Discs and vessels were visualized and subretinal abscess was noted in the macular area suggestive of endophthalmitis. After the core vitrectomy, she was instilled with intravitreal injection of 0.1 ml of amphotercin (5 μg) and 0.1 ml of voriconazole (100 μg). Again, vitreous tap was sent for microscopy and culture which also revealed A. flavus.

She was advised to continue topical voriconazole drops for every half an hour.

Blood culture was also sent which revealed no growth even after seven days of incubation. All her complete haemogram, liver function tests, serum creatinine, blood urea and blood glucose were normal. There was nothing abnormal detected in cardiovascular, respiratory and central nervous system examination. Her skin lesions were examined by a dermatologist. Skin scrapings were negative for fungal filaments. The skin lesions were diagnosed as tinea incognito. She was started with oral fluconazole 150 mg bd for her skin lesions for 15 days as advised by the dermatologist (liver function tests were normal). However, she took only two doses and stopped as she was not affordable. Five days after commencing voriconazole, one more vitreous tap was done and sent for microscopy and culture which was negative. The uveitis improved substantially during the first week of treatment, but there was no improvement in her visual acuity due to the macular involvement. Her visual acuity in the left eye was for hand movements only.

She was constantly advised to take voriconazole 1% eye drop, one drop half hourly, and moxifloxacin 0.5%, one drop every fourth hourly, and to review in retina clinic after a week. She was re-examined on subsequent visits, and she was instilled intravitreal 0.1 ml of voriconazole 100 μg for another three times. There was a marked reduction in the haziness of vitreous. Inflammation had settled. However, there was no further improvement in the visual acuity. There was no additional complaint. vitreous tap was again sent which also came negative for growth. She was asked to continue the treatment and to come for review after 15 days.


  Discussion Top


Aspergillus has a ubiquitous presence in the environment as a saprophytic mould isolated from soil and decaying organic matter. Aspergillus fumigatus and A. flavus are the most common species implicated in intraocular infection. There are many studies of Aspergillus species causing EE in immunocompromised individuals. However, a review of the literature revealed only a few cases of endogenous Aspergillus endophthalmitis (EAE) in immunocompetent patients.[6]

Usually, there are recognized risk factors which include a history of immunocompromised, malignancy, organ transplantation, long-term corticosteroid use, drug abuse, ocular surgery, trauma, endocarditis and chronic obstructive airway disease which can predispose to EE.

However, in some cases, EE can occur in a healthy individual without the source identified.

In our case, a comprehensive search for a portal of entry and a further focus of Aspergillus infection was conducted. However, we could not find any underlying immunocompromised condition. The probable route of entry, in this case, may be through the intravenous infusion which she had received two days before the ocular symptoms. However, unfortunately, we could not investigate the infusion bottles in the local hospitals. Since the patient is very young and no other associated risk factor, the fungaemia would have been checked by her immune cells efficiently, but unfortunately, the fungus has succeeded in reaching the eye resulting in endophthalmitis. There are many studies which have shown the occurrence of endophthalmitis through contaminated intravenous infusions. A study done by Nishanth et al.[7] has reported bilateral simultaneous EE in an immunocompetent individual caused by A. fumigatus. In this study also, there was no predisposing risk factor except one bottle of intravenous infusion in a local hospital. A study by Gupta et al.[8] reported EE in an immunocompetent individual caused by zygomycotic fungi. These authors also could not identify the source and they also had intravenous infusion history with dextrose infusions a week before the episode.

In cases of EE, blood culture is positive in only 33%. In our case also, there was no growth in blood culture.

The hallmark of EE is a significant involvement of the vitreous cavity. Vitreous involvement by Candida can present as vitritis or fluffy white retinal lesions extending into the vitreous, whereas Aspergillus can present as yellow/white lesions which can be focal or diffuse which was very classically seen in our case also.

Compared with published series of post-operative or post-traumatic endophthalmitis, patients with EE are more likely to have fungal isolates with a predominance of Candida albicans. EE is generally associated with high mortality and poor visual acuity outcomes, particularly when caused by more virulent species such as Aspergillus.

Fluconazole and Itraconazole are not useful in the treatment of Aspergillus endophthalmitis. Fluconazole is not active against Aspergillus species, and Itraconazole penetrates poorly into the eye.

Treatment for Aspergillus endophthalmitis classically involves intravitreal and/or systemic amphotercin, although the intraocular form has been associated with retinal toxicity. Voriconazole has good intraocular penetration. When used intravitreally, it may be safer than Amphotericin B. Pars plana vitrectomy is often performed for diagnostic and therapeutic purposes, especially when the diagnosis is unknown or the vision is severely compromised.[9]

In our case, we suspected the fungal aetiology on the day one of admission based on clinical presentation and started intravitreal voriconazole along with systemic therapy to ensure immediate achievement of the drug levels in the posterior segment.[10] Steroids were not given. Core vitrectomy was done to decrease the burden of organisms and to allow the removal of fungi that are inaccessible to systemic fungal agents.

In spite of early diagnosis and treatment, the visual acuity outcomes were very poor due to macular involvement. Her visual acuity was only for hand movements only. However, the early start of intravitreal voriconazole helped to clear the haziness in vitreous, and there was a marked reduction in inflammation.


  Conclusion Top


This case reveals one more EAE occurring in an immunocompetent individual. We could see that the drug voriconazole was effective against A. flavus. Although the visual acuity was not improved due to macular involvement, Voriconazole was helpful in limiting the further progression of infection. The case report also emphasizes the importance of early clinical suspicion of fungal endophthalmitis and appropriate institution of antifungal therapy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ramakrishnan R, Bharathi MJ, Shivkumar C, Mittal S, Meenakshi R, Khadeer MA, et al. Microbiological profile of culture-proven cases of exogenous and endogenous endophthalmitis: A 10-year retrospective study. Eye (Lond) 2009;23:945-56.  Back to cited text no. 1
    
2.
Connell PP, O'Neill EC, Fabinyi D, Islam FM, Buttery R, McCombe M, et al. Endogenous endophthalmitis: 10-year experience at a tertiary referral centre. Eye (Lond) 2011;25:66-72.  Back to cited text no. 2
    
3.
Essman TF, Flynn HW Jr., Smiddy WE, Brod RD, Murray TG, Davis JL, et al. Treatment outcomes in a 10-year study of endogenous fungal endophthalmitis. Ophthalmic Surg Lasers 1997;28:185-94.  Back to cited text no. 3
    
4.
Hosseini H, Saki S, Saki N, Eghtedari M. Aspergillus endophthalmitis in orthotopic liver transplantation. Indian J Med Sci 2009;63:253-6.  Back to cited text no. 4
[PUBMED]  [Full text]  
5.
Panigrahi PK, Roy R, Pal SS, Mukherjee A, Lobo A. Aspergillus terreus endogenous endophthalmitis: Report of a case and review of literature. Indian J Ophthalmol 2014;62:887-9.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Rana M, Fahad B, Abid Q. Embolic Aspergillus endophthalmitis in an immunocompetent patient from aortic root Aspergillus endocarditis. Mycoses 2008;51:352-3.  Back to cited text no. 6
    
7.
Sachdev N, Gupta P, Singh R, Chakrabarti A, Gupta V, Gupta A, et al. Bilateral simultaneous endogenous Aspergillus endophthalmitis in an immunocompetent patient. Retin Cases Brief Rep 2010;4:14-7.  Back to cited text no. 7
    
8.
Gupta P, Sachdev N, Kaur J, Dey P, Gupta V, Gupta A, et al. Endogenous mycotic endophthalmitis in an immunocompetent patient. Int Ophthalmol 2009;29:315-8.  Back to cited text no. 8
    
9.
Riddell J 4th, Comer GM, Kauffman CA. Treatment of endogenous fungal endophthalmitis: Focus on new antifungal agents. Clin Infect Dis 2011;52:648-53.  Back to cited text no. 9
    
10.
Sadiq MA, Hassan M, Agarwal A, Sarwar S, Toufeeq S, Soliman MK, et al. Endogenous endophthalmitis: Diagnosis, management, and prognosis. J Ophthalmic Inflamm Infect 2015;5:32.  Back to cited text no. 10
    




 

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