Article Text

Bilateral small retinal infiltrates during rickettsial infection
  1. JULIUS R LUKAS,
  2. STEFAN EGGER
  1. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  2. Department of General Medicine I, Section of Infectious Diseases, University Hospital Vienna, Austria
  3. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  1. BERNHARD PARSCHALK
  1. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  2. Department of General Medicine I, Section of Infectious Diseases, University Hospital Vienna, Austria
  3. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  1. MICHAEL STUR
  1. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  2. Department of General Medicine I, Section of Infectious Diseases, University Hospital Vienna, Austria
  3. Department of Ophthalmology and Optometry, University Hospital Vienna, Austria
  1. J R Lukas, Department of Ophthalmology and Optometry, University of Vienna, A-1090 Vienna, Waehringer Guertel 18-20, Austria.

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Editor,—Rickettsiae may cause heterogeneous retinal manifestations, the most characteristic of which are vascular lesions, periphlebitis, retinal haemorrhages and oedema, central retinal thrombosis, and papilloedema.1-5 We present the first case in which rickettsiae led to small retinal white infiltrates.

CASE REPORT

A previously healthy 25 year old woman had a fever up to 40°C of unknown origin during a trip to Queensland, Australia in August. Five days after the onset of fever a generalised maculopapular rash and a black lesion on the forefoot (eschar) were visible, without a known history of a tick bite. The patient was transferred to our hospital with the signs of general illness. Extensive examination for infectious disease including eye examination was initiated.

Visual acuity was 20/25 in both eyes. Slit lamp examination revealed bilateral conjunctival hyperaemia. Moderate inflammation of the vitreous in both eyes was visible. Fundus examination disclosed bilateral small white infiltrates within the neurosensory retina, practically without involvement of the choroid, mainly in the posterior pole (Fig 1). In the right eye, a tiny well defined haemorrhage near the temporal inferior artery was seen. Fluorescein angiography of both eyes showed punctuate hypofluorescence corresponding to the white infiltrates (Fig 2), staining of the optic discs, but no signs of vasculitis. Indocyanine green (ICG) angiogram, visual field examination, and colour tests were unremarkable in both eyes.

Figure 1

Fundus photograph of the left eye demonstrating multiple white spots in the posterior pole which were mainly confined to the neuroretina without any involvement of the choroid.

Figure 2

In the fluorescein angiogram these neuroretinal infiltrates blocked the background fluorescence throughout the whole phase of dye transit. (left eye, mid-phase, scanning laser ophthalmoscope).

Results of the following laboratory tests were pathologic: erythrocyte sedimentation rate (86 mm in the first hour), platelets (135 g/l), CRP (15 mg/dl), GOT (165 U/l), GPT (127 U/l), GGT (49 U/l), and LDH (527 U/l). Abdominal ultrasound sonography revealed an enlarged spleen (160 mm). The main serological finding was a definite increase of the Weil–Felix reaction from 1:160 (OX19, OX 2), 1:40 (OX K) to 1:1280 (OX 19, OX2) and 1:160 (OX K) within 1 week. Serology for brucella, salmonella, Yersinia enterocolica, Listeria monocytogenes, Mycoplasma pneumoniae,Francisella tularensis, Mycobacterium tuberculosis, Coxiella burnetti, Borrelia burgdorferi, Treponema pallidum, hepatitis (A, B, C), HIV, rubeola virus, rubella virus, Epstein–Barr virus, cytomegalovirus, herpes simplex I and II, Candida albicans, Cryptococcus neoformans,Aspergillus, toxoplasmosis, and chlamydia were all negative.

During antibiotic treatment with doxycycline 200 mg once daily for 14 days and clarithromycin 500 mg twice daily for 5 days, all symptoms subsided and the Weil–Felix reaction decreased to 1:640 (OX 19, OX2) and 1:80 (OX K). The visual acuity increased to 25/20 in both eyes. Four weeks after this treatment all laboratory tests were normal. Ophthalmic re-examination and angiography 3 weeks after initial presentation revealed improvement; 3 weeks later there was a complete resolution of retinal dots, and 6 months later findings were normal with no chorioretinal scars.

COMMENT

Based on patient history, clinical signs, and serology we concluded that the illness presented was associated with rickettsiae. Within the genus Rickettsia, small obligate intracellular bacteria, three groups of antigenically related organisms are known: spotted fever, typhus, and scrub typhus.6 7 Travel history, incubation time, and the marked titre increase of OX19 and OX2 indicate that the infectious agent was of the spotted fever group, most likelyRickettsia australis which occurs in Queensland, Australia. This rickettsia causes the Queensland tick typhus and its most prevalent vector is ixodic tick (Ixodes holocyclus,Ixodes tasmani).8 A bite by Ixodes tasmani may have been overlooked in the case presented, as, contrary to Ixodes holocyclus, the former is less apparent during feeding.8 Additional tests to specify the infectious agent unfortunately did not reveal any further clarification.

In general, rickettsiae invade endothelial cells, resulting in destruction of smooth muscle fibres, thrombosis, and extravasation of blood into the tissues.1-9 The papilloedema, also observed in our patient, is supposedly based on microvessel destruction.1 Further, rickettsiae may cause round cell infiltration in perivascular spaces in lungs, kidneys, brain, and adrenals.6 9 This is the first report to demonstrate small retinal infiltrates. The differential diagnosis of the ocular findings included many diseases which were excluded by serology. The complete resolution without any residual scars and normal ICG angiograms practically excluded chorioretinitis. Further, this retinitis did not meet the fluorescence-angiographic criteria of white dot syndrome, since no hyperfluorescence was observed. In conclusion, rickettsiae may lead to white dots in the retina and, thus, should be considered in the differential diagnosis.

References

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