Fig. 19.1
Post-cataract surgery Nocardia endophthalmitis. (Top left) Yellow-white nodule at surgical section and hypopyon; (top right) anterior chamber nodule with fibrin formation; (bottom left) yellow-white nodules at the tunnel site; (bottom right) nodules in the paracentesis site and tunnel site superiorly
One of the largest series of post-cataract Nocardia endophthalmitis described in the literature is a study of 24 cases that occurred over a 4-year period. This included 196 cases of postoperative endophthalmitis from 304,944 cataract surgeries. Nocardia endophthalmitis was suspected in cases based on the characteristic clinical features of yellow-white nodules in the anterior chamber (distinctive from bacterial and fungal). These cases presented early with a mean duration of 6 weeks [9]. In other reports of postoperative Nocardia endophthalmitis, the clinical presentation was also similar with fluffy white cotton ball-like exudates in the anterior chamber and exudates surrounding the intraocular lens and capsular bag [11, 15]. The presentation of Nocardia endophthalmitis after cataract surgery is generally thought to be late presenting even after a few months [16]. However, in other reports the presentation was much earlier, presenting even within 6 weeks of surgery [9, 17]. So Nocardia must be suspected in patients from endemic regions who present with an abscess or nodule at the incision site even if it presents early on in the course of the disease. The various clinical pictures of post-cataract surgery Nocardia endophthalmitis are shown in Fig. 19.1.
Cases with traumatic endophthalmitis may have more varied presentation depending on the severity of the trauma. But the characteristic feature of “fluffy white or yellow nodules” in the anterior chamber or on the iris will still be present [10]. Sometimes it could be overwhelming (Fig. 19.2).
Fig. 19.2
Traumatic endophthalmitis—the entire anterior chamber is filled with yellow-white nodules
Other reports of exogenous Nocardia endophthalmitis caused by new species are reported recently. In an immunocompetent child, endophthalmitis was caused by Nocardia kruczakiae after vegetable trauma presenting as late as 2 months [18]. Similarly, Nocardia farcinica causing infection of a Baerveldt implant and endophthalmitis in a patient with a Boston type I keratoprosthesis and Nocardia brasiliensis endophthalmitis in a patient with an exposed Ahmed glaucoma drainage implant are reported [19, 20]. In these cases the infection resolved with aggressive surgical and medical treatment.
Endogenous Endophthalmitis
Endogenous endophthalmitis occurrence is rare. It invariably occurs in immunocompromised patients. Nocardiosis is a serious life-threatening complication in immunosuppressed patients. In recent years isolated cases of Nocardia endogenous endophthalmitis have been reported. The clinical scenarios are varied from chronic steroid use and renal transplant [6, 7, 21–23]. It has also been reported as a rare sequel of pulmonary nocardiosis and from disseminated nocardiosis [24, 25]. Nocardia infection should be considered in any patient with atypical lung nodules and panuveitis. So patients who are systemically immunosuppressed are at greatest risk, and early suspicion of the role of this organism is paramount.
The first presenting sign of any systemic Nocardia infection may be ocular symptoms as is seen in many reports. In endogenous endophthalmitis signs are often limited to the posterior segment like panuveitis and yellowish, elevated subretinal lesion [21, 26]. Vitreous opacities and retinal detachments have also been described [6, 24]. Severe anterior chamber inflammation with fibrin formation is seen when the infection spreads to the anterior chamber.
Laboratory Diagnosis
Appropriate specimen selection is very important for proper isolation of Nocardia. The specimen must be representative of the disease. Haripriya et al. reported higher culture positivity with the anterior chamber aspirate in their series of post-cataract Nocardia endophthalmitis [9]. At the same time, the corneal and scleral specimens showed 100% positivity on the first sampling when the infection was confined to the surgical wound or in cases of scleral abscess [9]. Vitrectomy and a subretinal biopsy may be required for deep-seated infections. Conventional microscopy, culture, histopathology, and molecular diagnosis aid in confirming the etiological diagnosis [26]. However, it is not unusual for all specimens to be conventional culture negative and negative even by molecular tests since the 16S rRNA primer used for the universal identification of bacteria may not be sufficient to pick up Nocardia from ocular samples [27].
Specimens are inoculated directly onto 5% sheep blood agar, chocolate agar, brain heart infusion broth, and thioglycolate broth and incubated at 37 °C for 1 week. A Sabouraud dextrose agar is also inoculated and incubated at 25 °C for 2 weeks for fungal isolation. A direct microscopy for Gram stain, 10% potassium hydroxide, and a partial acid-fast stain must be done on the direct specimens.
On Gram stain, Nocardia is Gram-positive, bacillary, branching bacteria whose hyphae often fragment to coccobacillary forms (Fig. 19.3, top left). In 10% KOH wet mount, the filaments can be characteristically seen as thin filaments (Fig. 19.3, top right). A definite diagnosis is the detection of the organism directly from the specimen and growth on culture. As Nocardia is slow growing, plates have to be kept for extended period of time and regularly examined whenever Nocardia is suspected. Colony morphology may vary depending on the species, but most are described as chalky with colonies which may later produce colored pigments (Fig. 19.3, bottom left). Species-level identification is difficult for most of the microbiology laboratories, and this can be done in reference laboratories [1, 2].
Fig. 19.3
Laboratory diagnosis of Nocardia. (Top left) Gram-positive beaded filaments on Gram stain from a sample of aqueous humor; (top right) 10% potassium hydroxide wet mount showing Nocardia filaments; (bottom left) blood agar plate showing the characteristic chalky white colonies of Nocardia
All clinical significant isolates of Nocardia must be tested for antibiotic sensitivities. The common antibiotics tested against are amikacin, gentamicin, vancomycin, cefazolin, ceftazidime, ciprofloxacin, ofloxacin, and sulfonamides or trimethoprim-sulfamethoxazole. Antibiotic sensitivities can be done by the Kirby-Bauer disk diffusion method or by micro-broth dilution method. This is sometimes difficult for laboratories that do not do this regularly and may have to send it to a reference laboratory. The Clinical Laboratory Standards Institute (CLSI) has published an approved standard for susceptibility testing for both mycobacteria and aerobic actinomycetes [2, 28].
Treatment
Aggressive management is needed for control of the infections. Although Nocardia is a low virulent organism, it has a tendency to persist, and it is very difficult to eradicate. Vitrectomy, sector iridectomy of the iris mass with repeat injections of intravitreal antibiotics may be needed in the majority of cases. Intraocular lens extraction along with the bag may be the only way to limit the spread of infections in pseudophakic endophthalmitis.
Majority of endogenous Nocardia endophthalmitis has poor outcomes and often results in enucleation; there are also reports of death in extreme cases [22, 29]. There are exceptions, of course, when endogenous Nocardia endophthalmitis did not result in enucleation [6]. In many of these cases, delay in treatment due to initial misdiagnosis contributed to the morbidity and mortality. It is important that Nocardia be considered in the differential diagnosis in any immunosuppressed patient, including those receiving steroids, who presents with signs of intraocular infection.
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