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, 8th 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.

References

Chow, Jennifer K., et al. "Risk factors for albicans and non-albicans candidemia in the intensive care unit*." Critical care medicine 36.7 (2008): 1993-1998.

Harris, Anthony D., et al. "Risk factors for nosocomial candiduria due to Candida glabrata and Candida albicans." Clinical infectious diseases 29.4 (1999): 926-928.

Lee, Ingi, et al. "Risk factors for fluconazole-resistant Candida glabrata bloodstream infections." Archives of internal medicine 169.4 (2009): 379-383.

D M Mosdell, D M Morris, A Voltura, D E Pitcher, M W Twiest, R L Milne, B G Miscall, and D E Fry Antibiotic treatment for surgical peritonitis. Ann Surg. 1991 November; 214(5): 543–549.

Chow, Jennifer K., et al. "Factors associated with candidemia caused by non-albicans Candida species versus Candida albicans in the intensive care unit."Clinical infectious diseases 46.8 (2008): 1206-1213.

Chow JK, Golan Y, Ruthazer R, Karchmer AW, Carmeli Y, Lichtenberg DA, Chawla V, Young JA, Hadley S.Risk factors for albicans and non-albicans candidemia in the intensive care unit.Crit Care Med. 2008 Jul;36(7):1993-8.

Blumberg HM, Jarvis WR, Soucie JM, Edwards JE, Patterson JE, Pfaller MA, Rangel-Frausto MS, Rinaldi MG, Saiman L, Wiblin RT, Wenzel RP; National Epidemiology of Mycoses Survey(NEMIS) Study Group. Risk factors for candidal bloodstream infections in surgical intensive care unit patients: the NEMIS prospective multicenter study. The National Epidemiology of Mycosis Survey. Clin Infect Dis. 2001 Jul 15;33(2):177-86. Epub 2001 Jun 20.

Pappas PG, Kauffman CA, Andes D, Benjamin DK Jr, Calandra TF, Edwards JE Jr, Filler SG, Fisher JF, Kullberg BJ, Ostrosky-Zeichner L, Reboli AC, Rex JH, Walsh TJ, Sobel JD; Infectious Diseases Society of America.Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis. 2009 Mar 1;48(5):503-35. doi: 10.1086/596757.

Dimopoulos, George, et al. "Candida albicans versus non-albicans intensive care unit-acquired bloodstream infections: differences in risk factors and outcome." Anesthesia & Analgesia 106.2 (2008): 523-529.

Edmond, Michael B., et al. "Nosocomial bloodstream infections in United States hospitals: a three-year analysis." Clinical infectious diseases 29.2 (1999): 239-244.

Pfaller, Michael A., et al. "Epidemiology and outcomes of invasive candidiasis due to non-albicans species of Candida in 2,496 patients: data from the Prospective Antifungal Therapy (PATH) registry 2004–2008." PloS one 9.7 (2014): e101510.

Diekema, Daniel, et al. "The changing epidemiology of healthcare-associated candidemia over three decades." Diagnostic microbiology and infectious disease 73.1 (2012): 45-48.

Méan, Marie, Oscar Marchetti, and Thierry Calandra. "Bench-to-bedside review: Candida infections in the intensive care unit." Crit Care 12.1 (2008): 204.

Ostrosky-Zeichner, Luis, and Peter G. Pappas. "Invasive candidiasis in the intensive care unit." Critical care medicine 34.3 (2006): 857-863.

Lashof, AML Oude, et al. "Duration of antifungal treatment and development of delayed complications in patients with candidaemia." European Journal of Clinical Microbiology and Infectious Diseases 22.1 (2003): 43-48.

Fishman, Louis S., et al. "Hematogenous Candida endophthalmitis—a complication of candidemia." New England Journal of Medicine 286.13 (1972): 675-681.

Pagano, Livio, et al. "Chronic disseminated candidiasis in patients with hematologic malignancies. Clinical features and outcome of 29 episodes."haematologica 87.5 (2002): 535-541.

Murray, Henry W., Mark A. Fialk, and Richard B. Roberts. "Candida arthritis: a manifestation of disseminated candidiasis." The American journal of medicine60.4 (1976): 587-595.

Falcone, Marco, et al. "Candida infective endocarditis: report of 15 cases from a prospective multicenter study." Medicine 88.3 (2009): 160-168.

Franquet, Tomás, et al. "Pulmonary Candidiasis after Hematopoietic Stem Cell Transplantation: Thin-Section CT Findings 1." Radiology 236.1 (2005): 332-337.

Kontoyiannis, D. P., et al. "Hepatosplenic candidiasis: a manifestation of chronic disseminated candidiasis." Infectious disease clinics of North America14.3 (2000): 721-739.

Pastakia, B., et al. "Hepatosplenic candidiasis: wheels within wheels."Radiology 166.2 (1988): 417-421.

Anttila, Veli-Jukka, et al. "Hepatosplenic candidiasis in patients with acute leukemia: incidence and prognostic implications." Clinical infectious diseases24.3 (1997): 375-380.

Hamilton, Keith W., and Ebbing Lautenbach. "Candidemia in the Intensive Care Unit.Healthcare Associated Infections: A Case-based Approach to Diagnosis and Management (2013).