Pathogenesis and clinical presentation

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Invasive candidiasis is not a single syndrome, rather a spectrum of infections that differ in terms of clinical presentation and course depending on the type of host immune immunosuppression. Many forms of invasive candidiasis are potentially severe, however, with high (30-60%) rates of crude morbidity and mortality.19 The most common form of invasive candidiasis is seen in non-neutropenic patients with disruption of the GI, skin or microbiologic barriers giving rise to a bloodstream infection (fungemia) from, or seeding to, a central venous catheter. Catheter-related candidemia carries a good prognosis if appropriate antifungal therapy is instituted early with catheter removal.1 Fungemia can be of high density, however, leading to metastatic sites of infection and invasion of deep organs with increased morbidity. Therefore, the infection must be taken seriously, especially in patients with poor performance status (i.e., a high Acute Physiology, Age, and Chronic Health Evaluation II score) in the ICU.

Patients with acute disseminated candidiasis share many similar features as patients with catheter-related candidemia, except infection generally arises from the gut following mucotoxic chemotherapy and the patients are often pro foundly ill. Hematogenous spread to noncontiguous organs is common in patients with acute disseminated candidiasis, and outcome is heavily dependent upon recovery from neutropenia.19 Fluconazole prophylaxis has markedly decreased the incidence of acute disseminated candidiasis among high-risk patient groups such as bone marrow transplant and acute leukemia patients. 9 However, breakthrough infections with fluconazole-resistant C. glabrata and C. krusei are still a concern.

Some forms of invasive candidiasis are dominated by deep-organ infection and may never be detected by blood cultures. Chronic disseminated candidiasis or hepato-splenic candidiasis is a unique presentation of candidemia seen after recovery from neutropenia. Candidemia during the period of neutropenia may be initially localized to the portal circulation with dissemination to contiguous organs. After recovery of neutrophils, an inflammatory response is seen against areas of focal infection in the liver and spleen. This inflammatory response produces abdominal pain that is associated with increases in alkaline phosphatase levels and hepatocellular enzymes.19 Diagnosis is typically confirmed by patient history (recent neutropenia), and multiple areas of lucency in the liver and spleen on CT.

Focal invasive candidiasis has been reported for virtually every organ, even following apparently uncomplicated catheter-related fungemia. The most common sites of infection are the kidney, eye, and bone. Candida in the urine can be an indication of renal candidiasis or an obstructing fungus ball; however, it must be distinguished from more benign colonization of the urinary tract, especially in patients with chronic indwelling urinary catheters.19 All patients with candidemia should undergo an eye exam to rule out Candida endophthlamitis, which can be sight-threatening if not recognized early.19

Invasive Candidiasis Morbidity
FIGURE 84-3. Opportunistic mycoses in clinical samples. A. Candidiasis (tissue). B. Cryptococcosis (India ink stain of CSF). C. Aspergillosis (tissue). D. Zygomycosis (tissue).

Laboratory diagnosis of invasive candidiasis is established by detection of the yeast in blood cultures or another sterile site (Fig. 84-3A)19. Growth of Candida from urine, sputum, or respiratory secretions (including bronchoalveolar lavage) is not considered to be evidence of invasive infection, as these areas frequently become colonized with Candida species in patients receiving broad-spectrum antibiotics.19 Colonization at multiple distinct body sites or with high density of Candida species, however, may precede invasive infection. Therefore, preemptive antifungal therapy may be indicated in colonized high-risk populations such as those with neutropenic fever, transplant recipients, or following major abdominal surgery.19 Although Candida are not particularly fastidious organisms, the sensitivity of blood cultures is relatively poor (less than 60%) and a negative culture does not rule out infection.19 The poor sensitivity of blood cultures for detecting invasive disease has led to the study of novel serodiagnostic tests to detect antibodies, fungal metabolites, fungal cell wall antigens, or nucleic acids of Candida species. Of the four approaches, antigen testing based on the detection of ^-glucan polymers in the cell wall of Candida have appeared most promising; however, none ofthese diagnostic tests have achieved routine clinical use.

Laboratory identification of Candida in clinical samples must be performed to the species level whenever possible, as Candida species differ considerably in their susceptibility to antifungal agents.19,20 Rapid discrimination of C. albicans from common nonalbicans Candida species can be accomplished by the germ-tube test, which presumptively identifies C. albicans by the early formation (less than 4 hours) of a hyphae-like structure when the yeast in incubated in serum at 37°C (98.6°F). Definitive species identification, however, may require an additional 48 to 72 hours after the organism is isolated on agar. Fluorescent in situ hybridization (FISH) of Candida species-specific DNA sequences can reduce the time needed for definitive species identification, but is not available at most hospitals.

C. albicans remains the most common cause of invasive candidiasis, is the most virulent of Candida species, but is the most susceptible to commonly used antifungals including fluconazole.19,20 Like C. albicans, C. tropicalis is a relatively virulent species that has a tropism for causing deep tissue invasion. C. tropicalis is generally sensitive to antifungals including fluconazole.19,20 C. parapsilosis is a less virulent species seen frequently in neonates and in adults with central venous catheters. Although C. parapsilosis is less virulent, many isolates form thick biofilms on prosthetic materials and catheters that make the organism difficult to eradicate.19,20 C. parapsilosis is generally susceptible to most antifungals including fluconazole. However, higher dosages of echinocandins (e.g., 70-100 mg/day of caspofungin) have been suggested due to the decreased potency of the echinocandin class against this species. C. krusei is a less-common species associated with breakthrough infections in heavily immuno-compromised patients and should always be considered resistant to fluconazole.19,20 Interestingly, most fluconazole-resistant isolates of C. krusei retain susceptibility to itraconazole and voriconazole, based on laboratory analysis.

C. glabrata has become a common cause of both de novo candidemia in heavily immunocompromised hosts and breakthrough infection in patients on fluconazole prophylaxis. Although C. glabrata is less virulent than other Candida species, infections with this organism are typically seen in patients with poor performance status, therefore mortality remains high. The marginal susceptibility of C. glabrata to fluc-onazole dictates that other agents such as amphotericin B or the echinocandins be considered as first-line therapy until susceptibility to fluconazole can be documen-ted.19,20 The effectiveness of voriconazole or posaconazole for fully fluconazole-res-

istant C. glabrata fungemia is not well established, and cross-resistance among these


triazole antifungals has been documented in laboratory studies. '

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Cure Your Yeast Infection For Good

Cure Your Yeast Infection For Good

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