Within invasive fungal sinusitis there are two distinct subtypes, acute and chronic. Acute sinusitis occurs in immunocompro-mised hosts (bone marrow transplant patients, HIV, etc.) and generally lasts for less than 4 weeks. In the literature it is commonly referred to as fulminant sinusitis, conveying the rapid disease progression and destruction affiliated with the infection (Ferguson, 2000a). Characteristically the disease progresses in a matter of days, with hyphal growth and extension pushing out of the sinus cavities and invading the surrounding mucosa, vascular system, and in severe cases, the cranium. Histological analysis reveals prominent hyphal extension, an influx of cellular exudates, and necrotic tissue surrounding the area. If patients presenting symptoms of acute invasive sinusitis fail to receive proper medical treatment, severe damage can occur to the nasal cavity, bone structure, and death can ensue (Fig. 1.2).
In studies performed by Rudack on mucosa samples from acute invasive sinusitis patients, concentrations of proinflamma-tory cytokines interleukin (IL)-ip and IL-6 were shown to be increased compared to control mucosa, but not seen at levels high enough to merit statistical significance (Rudack et al., 1998). However in analyzing levels of IL-3 and IL-8, values were significantly higher than controls, indicating an innate immune response against the invading fungus.
Most cases of acute sinusitis begin with the onset of the common cold (NIAID, 2002). These viral colds do not cause acute sinusitis per se, but rather act to inflame the sinuses and surrounding mucosa. Even if immunocompromised, most hosts would still be able to clear fungal spores from the nasal cavity via ciliated cells (Baraniuk, 1994). However with the overproduction of mucus and increased inflammation caused by the cold, the size of the ostium becomes limited, and any fungi present in the sinuses can no longer be mediated effectively. This is also the case for other opportunistic organisms such as Haemophilus influenzae and Streptococcus pneumoniae (NIAID, 2002).
Again, the most predominant organisms seen within this disease state are A. fumigatus, A. flavus, and species of Alternaria (Table 1.1). Additionally rare cases of Cryptococcus neoformans and Candida albi-cans have been seen in cases of acute invasive fungal sinusitis (Schell, 2000).
Chronic fungal sinusitis differs from the acute variation in that the host is for the most part immunocompetent and the symptoms affiliated with the disease last longer than 4 weeks (Washburn, 1994).
These patients typically suffer from a longstanding history of upper respiratory allergies, asthma, and nasal polyposis. The disease can take months or years to progress and symptoms include the erosion of barriers separating the paranasal cavities, as well as adjacent structures such as the orbits, brain, and pituitary gland (Stringer, 2000). Additionally patients suffer from mycotic aneurysms, carotid artery ruptures, erosion of the maxillary floor which results in palatal degradation, and erosion of the cribriform plate which results in chronic headaches, seizures, and decreased mental status. Etiological agents found in clinical cases are the same as those in the noninvasive and the acute invasive forms (Schell, 2000).
In studies performed by Rudack and others on samples taken from chronic fungal sinusitis patients, the only cytokine shown at elevated levels was IL-3 (Rudack et al., 1998). This is contrasted against more recent work which indicates the increased expression of IL-1P, IL-5, IL-6, IL-8, and TNF-a in the sinonasal mucosa of patients with chronic sinusitis (Lennard et al., 2000).
The exact etiology of what causes chronic invasive fungal sinusitis is unknown. Most patients are immunologically intact and contain no cellular level defects that contribute to the overall morbidity of the disease (Washburn, 1994). The chronic inflammation results in rearrangement of the normal sinus architecture, which impedes drainage and can lead to superimposed bacterial sinusitis (Ferguson, 2000a). However, the notion of this pathophysiol-ogy being sufficient to cause chronicity is unfounded. One report suggests that the fungus is simply acting as an opportunist and taking advantage of a weakened and diseased sinus and yet others point to the not yet fully elucidated fungal virulence factors as rationale (Jahrsdoerfer et al., 1979).
Chronic invasive fungal sinusitis is usually misdiagnosed and is only recognized after patients take antibiotics for a long period without cessation of symptoms (Stringer, 2000). Current therapy uses the prescription of steroids to initially decrease inflammation, and if no change is seen in the patient's progress, a combination of endo-scopic surgery and antifungal chemotherapy is applied. Even with these procedures the disease state recurs quite frequently post-surgery and posttreatment (Washburn, 1994; Stringer, 2000; NIAID, 2002).
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