Candida - albicans and non-albicans

The presence of Candida glabrata in the blood cultures is explored in Question 18 from the second paper of 2011.

Microbiology of albicans and non-albicans Candida species

Some of this information can be found in J.E.Edwards' Chapter 258 of Principles and Practice of Infectious Diseases, 8^th ed. (2015)

Specific features of importance are summarised below.

• Candida species are yeasts, i.e. fungi which exists predominantly in a unicellular form.
• They grow reasonably well in routine culture bottles, and therefore there is no need for any sort of special "fungal cultures".
• The cells stain gram positive.
• They are normal commensurals (your are practically covered in their hyphae right now)
• Neutrophils are the key to defence against these yeasts, and neutropenia is a major risk factor for disseminated candidiasis.

Risk factors for developing a non-albicans candidaemia

A good article on this exact subject is available. It had found that non-albicans candidaemia is associated with CVCs and multiple antibiotic therapy. TPN also seems to all but triple the risk of non-albicans candidaemia. There is also an association with malignancy, which is biased by the fact that most studies of candidaemia have been performed in solid or hematological cancer patients. Renal failure is another significant risk factor.

Thus, in summary, risk factors for non-albicans candidaemia are as follows:

Among immunocompetent patients:

• Repeated abdominal surgeries
• Exposure to broad-spectrum antibiotics
• Exposure to fluconazole
• Diabetes
• CVC insertion
• TPN use
• Malignancy
• Renal failure

Among immunosuppressed patients, non-albicans candidaemia occurred more frequently in those with medical devices or receiving steroids, and was associated with higher mortality.

It is probably impossible to discriminate between albicans and non-albicans candidaemia on the basis of clinical characteristics alone. However, the prior use of fluconazole may select for a fluconazole-resistant species such as C.glabrata, so that could be viewed as a discriminating characteristic. This issue is rapidly becoming a non-issue. The point of discriminating between the two candidaemias has tradidtionally been a question of "will it/won't it respond to fluconazole". But the prevalence of non-albicans candidaemia in some parts of the world now contributes up to 50% of all candidaemias, and Candida albicans species are acquiring fluconazole resistance.

Complications of candidaemia in general

Generally speaking, these are delayed complications, resulting from haematogenous deposition of Candida organisms around the body. They typically lodge in solid organs, and grow into fungus balls, invading and destroying tissue. A book chapter (by Hamilton and Lautenbach, from Healthcare Associated Infections: A Case-based Approach to Diagnosis and Management, 2013) describes these complications in brief; a summary with references is offered below.

According to a good summary article from 2003, major risk factors for delayed complications seem to be neutropenia, prostheses, and a poor initial response to treatment. These people need longer than the usual two weeks of antifungals - perhaps up to six weeks in total. Generally speaking, unless you recover your neutrophil function, disseminated "metastatic" candidasis is uniformly fatal.

Candida endophthalmitis (specifically, retinitis) is enough of a problem for the Infectious Diseases Society of America to issue recommendations regarding early retinal examination for these patients. It was described in a good 1972 article; the patients developed this complication between three and fifiteen days after their first positive candida blood cultures.

Candida endocarditis is the most feared complication, and it seems that the most common pathogen (28%) is a non-albicans species. The in-hospital mortality seems to be high, up to 46% even today, and 80%-100% in historical case series.

Candida arthritis tends to occur as a primary infection of the joint or bursa. From case reports, one can surmise that non-operative treatment may be successful.

Pulmonary candidiasis, when caused by embolic rather than native pulmonary infection, tends to manifest as cavitating lung lesions and is generally hideous. Initially, nodules on CT are the major finding; they may be surrounded by a halo of ground-glass opacity, representing an area of oedema and haemorrhage.

Hepatic and splenic candida abscesses tend to form in neutropenic or chronically immunosuppressed patients, and are increasing in incidence. In these patients, death is frequently attributed to other causes, and there is a population who can sustain continuous antifungal therapy for months with "indolent" suppressed abscesses and little organ dysfunction.