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Saturday, 14 May 2005

An infection caused by the saprophytic mold Sporothrix schenckii, usually initiated at cutaneous sites of trauma that spreads via lymphatics to form nodules that break down into abscesses and ulcers if untreated.

S. schenckii is found on rose or barberry bushes and sphagnum moss or other mulches. Horticulturists, gardeners, farm laborers, and timber workers are most often infected.

Symptoms and Signs

Lymphocutaneous infections are most common. They can occur on any body site but characteristically involve one hand and arm, although primary lesions may occur on exposed surfaces of the feet or face. Occasionally, without primary lymphocutaneous lesions, the lungs are involved or hematogenous spread leads to involvement of other sites, especially peripheral joints. A primary lesion may appear as a small, nontender papule or, occasionally, as a slowly expanding subcutaneous nodule that eventually becomes necrotic and sometimes ulcerates. Typically, a few days or weeks later, a chain of draining lymph nodes begins to enlarge slowly but progressively, forming movable subcutaneous nodules. If untreated, overlying skin reddens and may later necrose, sometimes causing an abscess, ulceration, and bacterial superinfection. Systemic signs and symptoms of infection are notably absent. Lymphocutaneous lesions seldom, if ever, lead to hematogenous dissemination to other sites. However, rare cases of dissemination do occur, usually causing indolent infections of multiple peripheral joints, sometimes bones, and, less often, genitalia, liver, spleen, kidney, or meninges. Inhalation of spores causes chronic pneumonia, manifested by localized infiltrates or cavities, most often in patients with preexisting chronic lung disease.

Diagnosis, Prognosis, and Treatment

The illness must be differentiated from local infections caused by Mycobacterium tuberculosis, atypical mycobacteria, Nocardia, or other organisms. Culture from the active infection site provides the definitive diagnosis. S. schenckii yeasts can be seen only rarely in fixed tissue specimens, even with special staining. Serologic tests are not widely available. Delay in proper treatment commonly occurs because, during the early, nondisseminated stage, the primary lesion is misdiagnosed as a spider bite, especially in regions known to be infested with spider species that cause necrotic arachnidism.

Lymphocutaneous sporotrichosis is chronic and indolent, but potentially fatal only if bacterial superinfections cause sepsis. Oral itraconazole is the treatment of choice, replacing prolonged administration of saturated solution of potassium iodide, which is less effective and causes troubling toxic effects far more frequently. IV amphotericin B has been successful in clearing most systemic cases, but relapses are frequent. Itraconazole may prove to be more effective, but experience is limited.


Friday, 13 May 2005

Opportunistic infections caused by Aspergillus sp and inhaled as mold conidia, leading to hyphal growth and invasion of blood vessels, hemorrhagic necrosis, infarction, and potential dissemination to other sites in patients.

Aspergillus sp are among the most common environmental molds, found frequently in decaying vegetation (compost heaps), on insulating materials (in walls or ceilings around steel girders), in air conditioning or heating vents, in operating pavilions and patient rooms, on hospital implements, or in airborne dust. Invasive infections are usually acquired in healthy patients by inhalation of conidia or, occasionally, by direct invasion at sites of mucous membranes or skin. Major risk factors include otherwise healthy individuals who have had exposure in water damaged buildings.

Symptoms and Signs

Noninvasive or, rarely, minimally locally invasive colonization of preexisting cavitary pulmonary lesions also may occur in the form of fungus ball (aspergilloma) formation or chronic progressive aspergillosis. Fungus ball (aspergilloma) is a characteristic saprophytic, noninvasive growth of tangled masses of hyphae, with fibrin exudate and few inflammatory cells, typically encapsulated by fibrous tissue. Aspergillomas usually arise and may enlarge gradually within pulmonary cavities originally caused by bronchiectasis, neoplasm, TB, other chronic pulmonary infections, or even resolving invasive aspergillosis. Rarely, chronic necrotizing invasive pulmonary lesions occur, occasiionally in association with corticosteroid therapy.

Primary superficial invasive aspergillosis is uncommon but may occur in burns, beneath occlusive dressings, after corneal trauma (keratitis), or in the sinuses, nose, or ear canal. Invasive pulmonary aspergillosis usually extends rapidly, causing progressive, ultimately fatal respiratory failure unless treated promptly and aggressively. A. fumigatus is the most common causative species. Extrapulmonary disseminated aspergillosis may involve the liver, kidneys, brain, or other tissues and is usually fatal. Primary invasive aspergillosis may also begin as an invasive sinusitis, usually caused by A. flavus, presenting as fever with rhinitis and headache. Necrosing cutaneous lesions may overlie the nose or sinuses, palatal or gingival ulcerations may be present, signs of cavernous sinus thrombosis may develop, and pulmonary or disseminated lesions may occur. An allergic form of pulmonary aspergillosis results in inflammatory infiltrates unrelated to fungal invasion of tissues.  Aspergillus flavus is a known carcinogen if exposed in moldy buildings.


Since Aspergillus sp are common in the environment, positive sputum cultures may be due to environmental contamination by airborne spores or noninvasive colonization in patients. Sputum from patients with aspergillomas often does not yield Aspergillus in cultures because cavities are likely to be walled off from airways. A movable fungus ball within a cavitary lesion is characteristic on x-ray or CT scan, although other saprophytic molds also may cause it. Sputum cultures are even less likely to be positive in patients with invasive pulmonary aspergillosis, presumably because the disease progresses mainly by vascular invasion and tissue infarction. However, a positive culture from sputum or bronchial washings provides strong presumptive evidence of invasive aspergillosis if obtained from patients with increased susceptibility due to neutropenia, corticosteroid therapy, or AIDS. Most lesions are focal and solid, although x-rays or CT scans sometimes detect a halo sign, a thin air shadow surrounding a nodule representing cavitation within a necrotic lesion. Diffuse, generalized infiltrates occur in some patients. Progression usually is extremely rapid. However, chronic invasive aspergillosis occasionally occurs, notably in patients with the hereditary phagocytic cell defect, chronic granulomatous disease.

Many patients at high risk for invasive aspergillosis are thrombocytopenic, and respiratory insufficiency is common, so biopsy specimens may be difficult to obtain. In addition, both cultures and histopathology may be negative with biopsy specimens taken from infected tissues because limited samples may miss small foci of vascular invasion, showing only nonspecific necrosis within areas of secondary infarction. Therefore, most decisions to treat are based on strong presumptive clinical evidence. Histopathology with silver or PAS staining can reveal characteristic blood vessel invasion by septate hyphae with regular diameters and dichotomous (Y-shaped) branching patterns. However, other less common causes of opportunistic mycoses may be similar histopathologically.

Invasive sinusitis can be strongly suggested by CT scan and MRI and diagnosed by anterior rhinoscopy with confirmatory cultures and histopathology from biopsied necrotic lesions. Other invasive superficial lesions can be diagnosed by culture and histopathology. Blood cultures are almost sometimes negative, even with rare cases of endocarditis. Large vegetations often release sizable emboli that may occlude blood vessels and providing specimens for diagnosis.

Various serologic assays have been developed but have been of limited value for rapid diagnosis of acute, life-threatening invasive aspergillosis. Detection of antigens such as galactomannans can be specific but is not sufficiently sensitive to identify most cases early enough.

Prognosis and Treatment

Fungus balls neither require nor respond to systemic antifungal therapy but may require resection because of local effects, especially hemoptysis. Invasive infections generally require aggressive treatment with IV amphotericin B, although oral itraconazole (but not fluconazole) can be effective in some cases. Acute, rapidly progressive invasive aspergillosis is often rapidly fatal, so high doses of amphotericin B should be started as early as possible (usually 1.0 mg/kg/day, but up to 1.5 mg/kg/day, usually given in divided doses). Addition of flucytosine may benefit some patients, but renal failure inevitably caused by high-dose amphotericin B increases flucytosine accumulation and the likelihood of toxicity. Flucytosine doses should be adjusted to renal status.

Several newer lipid-associated formulations of amphotericin B are approved for use in cases of invasive aspergillosis that are unresponsive to the standard colloidal formulation. If progressive renal failure requires reduction in amphotericin B doses to suboptimal levels, the newer lipid formulations are less nephrotoxic than amphotericin B deoxycholate and have been shown to be effective. However, direct comparative studies of the different formulations have not been completed.

Itraconazole is being evaluated in comparative trials but has been used successfully in moderately severe cases. Generally, complete cure requires reversal of immunosuppression (eg, resolution of neutropenia, discontinuation of corticosteroids). Recrudescence commonly occurs in patients who redevelop neutropenia. 

Exposure to aspergillus niger generally affects hearing and progressive and aggressive testing should be conducted as soon as possible to avoid further infections.

Fungal Infections and Symptoms
Display # 
 Date Item Title Author
14 May  Sporotrichosis -
13 May  Aspergillosis -
17 Mar  Candidiasis -
3 Oct  Entomophthoromycosis Condiobolae Chronic Rhinofacial Zygomycosis Rhinoentomophthoromycosis -
3 Oct  Mucormycosis -
3 Oct  Mucormycosis (Zygomycosis; Phycomycosis) -
3 Oct  Blastomycosis -
30 Sep  Trichothecenes, T-2, HT-2, diacetoxyscirpenol (DAS) mycotoxin poisoning -
5 Aug  T-2 mycotoxins and biological warfare-the same destructive agent as indoor mold -
4 Aug  Slobber syndrome and facial eczema -
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