Ocular infections caused by Moraxella sp have an interesting social history, often with somewhat unsavoury associations. To begin with, Moraxella is a true ophthalmic pathogen, an “eye bug” par excellence that can occasionally be found colonising the nasopharynx and on other mucous membranes,¹ although rarely causing infections in other parts of the body. Originally isolated by Morax² and Axenfeld³ in 1896 and 1897, respectively, from patients with angular blepharitis, the organism was at first called the diplobacillus of Morax–Axenfeld, and later came to be known as M lacunata. In 1899, Petit⁴ isolated a similar organism from a central corneal ulcer that he called, not surprisingly, the diplobacillus of Petit. This organism was later renamed M liquefaciens. A third species was also isolated, M nonliquefaciens, which was felt to be more benign, rarely causing keratitis or severe ocular infections. These rather arbitrary divisions into different species were based on the degree of liquefaction produced by the organisms when they were inoculated on to coagulated human serum, known as Loeffeler’s medium.

In 1900, Moraxella sp was reported by several authors to be the most common cause of conjunctivitis in Europe.⁵ But by the middle of the century, Thygeson and Kimura,⁶ Jones et al⁷ and others reported that the organism could be cultured in ⩽1% of all cases of conjunctivitis, an apparent dramatic decline in the prevalence of Moraxella ocular infections in the population. The organism was down but still not out. A common view at the time was that different species of the organism selectively grew only in specific areas of the external eye. Angular blepharitis was thought to be caused by M lacunata, whereas corneal ulcers were said to be almost always caused by M liquefaciens.⁸ This view persisted until 1980, when Baum et al⁵ reported 20 cases of Moraxella keratitis in 19 patients from a derelict population in New York city. M lacunata was grown from the ulcers of only two of the patients, whereas M liquefaciens was cultured from seven, M nonliquefaciens from eight and mima Moraxella from three. In effect, Baum showed that the species of the organism causing corneal ulceration was irrelevant. What mattered clinically was that the bacteria produced destructive proteases and endotoxins, and this ability was exhibited by all of the species in question.

Baum et al also reiterated what was believed to be one of the more unsavoury characteristics of Moraxella organisms, their apparent predilection for colonising alcoholics and derelicts and causing corneal ulceration almost exclusively in these patients. We now know that this is not necessarily the case. Moraxella can cause keratitis in any compromised host, including those dependent on alcohol, but normal people can be infected as well, especially if they have a persistent corneal epithelial defect or corneal pathology that enhances their susceptibility. Moraxella is an opportunist. It can be cultured from many sites in the body, but it rarely causes clinical disease unless it infects the eye—its preferred host.

The organism is amazingly indolent from the laboratory point of view. Most biochemical tests performed on the bacterium are negative; however, it does share one positive test in common with its more virulent relatives. Similar to Pseudomonas sp, Neisseria meningitidis and N gonorrhoeae, the Moraxella genus is oxidase positive. Like them it is also Gram negative, and sometimes its large pink dipplobacilli, which have been described as looking like big box cars, are so pleomorphic that it is possible for a microbiologist to confuse the morphology with that of Neisseria sp. This raises an interesting question about how closely these organisms are actually related.

A case in point is the curious family history of N catarrhalis. The runt of the Neisseria genus from birth, N catarrhalis never felt at home. His big pushy sisters, N gonorrhoeae and N meningitidis, produced their own diseases and occasionally even thumbed their noses at antibiotic treatment. To be sure, N catarrhalis was oxidase positive and liked to grow on chocolate agar, but he could never figure out how to use sucrose, not to mention dextrose or maltose; and he had no disease that he could call his own except for the occasional opportunist eye infection. This sad state of affairs was finally set right by a kindly well-meaning taxonomist,⁹ whose breed should be recognised as the social workers of microbiology. N catarrhalis was moved to the Branhamella genus and rechristened B catarrhalis. For awhile things went well, but unfortunately Bcatarrhalis just never fitted in with the kindly Branhamella clan. There was no excitement at all compared with his boisterous Neisseria family, and Bcatarrhalis slowly languished as runts and misfits often do. To remedy this unhappy situation the taxonomists moved him once more, this time to the Moraxella genus. He was christened yet again (one would hope for the last time) as M catarrhalis, and there he remains in the Moraxella family to this day. Admittedly, it’s a boring existence, causing only the occasional acute or chronic catarrhal conjunctivitis, the odd opportunist corneal ulcer and the rare pseudo membrane.⁸ It’s not much of a life, but it may be all that a bug like M catarrhalis can ever expect as a temporary guest in the Moraxella clan. Of course, the issue of his true paternity is still not decided, even though it is now possible to determine it with DNA testing. When that occurs, and the genetically related relatives of M catarrhalis are finally tracked down, it is very likely that he may have to pack up and move again. C’est la vie. It is a bug-eat-bug world out there.

My apologies for the frivolity of this digression and any microbiological disrespect it might imply, but the point is to illustrate how the association of an apparently docile bacterium with truly pathological relatives may explain how that organism can produce a virulent clinical infection. In the case of corneal ulcers caused by Moraxella sp, even though the organism is described as being clinically indolent it can also be extremely destructive to corneal tissue. The keratitis it produces usually deepens rather than spreading peripherally, and the associated inflammatory response can be so hyperacute that a hyphema forms within a hypopyon—a clinical feature that is usually seen in ulcers infected with much more virulent bacteria. Moraxella is also paradoxically sensitive to most antibiotics, and resistant strains rarely develop. Yet the clinical course of a Moraxella corneal ulcer can be uncommonly protracted and fraught with many complications. Even though the ulcer is almost always rapidly sterilised in the first few days of treatment, the destruction of the corneal tissue continues unabated, sometimes for weeks, requiring the addition of topical corticosteroids and other adjunctive therapeutic agents to prevent severe corneal necrosis and perforation. Even in its response to treatment it can be said that a Moraxella corneal ulcer often appears to be down but it is never out. Once the diagnosis is confirmed with positive corneal scrapings and cultures, the truly difficult part begins: the battle to limit the necrosis of the corneal tissue that ultimately leads to scarring and visual disability. In this sense Moraxella can truly become the bug from hell.

My congratulations to Das et al¹⁰ for providing in this issue of the British Journal of Ophthalmology (see p 1236) an excellent analysis of 95 cases of culture-proved Moraxella keratitis. The authors have shown that multiple local ocular risk factors predispose a person to Moraxella keratitis. This was the case in 78 of the 95 eyes (table 1 in Das et al¹⁰). Systemic risk factors such as diabetes, rheumatoid arthritis and leprosy were also mentioned in 13 patients (table 2 in Das et al¹⁰). It is of interest that terms such as alcoholic and derelict were not mentioned even once in this article as predisposing a person to Moraxella keratitis. This series of patients appears to finally put to rest the myth that Moraxella keratitis is a disease seen only in those who are alcoholic, derelict, or down and out. It is obvious from this excellent study that the organism is merely an opportunist looking for a compromised host, and its preferred host can be any cornea that is locally compromised for any number of reasons.