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A fungus is a member of a large group of eukaryotic organisms that includes microorganisms such as yeasts and molds (British English:

moulds), as well as the more familiar mushrooms. These organisms are classified as a kingdom, Fungi, which is separate from plants, animals, and bacteria. One major difference is that fungal cells have cell walls that contain chitin, unlike the cell walls of plants, which contain cellulose. Characteristics of fungi eukaryotic, non- vascular organisms reproduce by means of spores, usually wind-disseminated both sexual (meiotic) and asexual (mitotic) spores may be produced, depending on the species and conditions typically not motile, although a few (e.g. Chytrids) have a motile phase. Moving or having the power to move spontaneously like plants, fungi have an alternation of generations fungi are heterotrophic ( other feeding, must feed on preformed organic material), not autotrophic ( self feeding, make their own food by photosynthesis). Unlike animals (also heterotrophic), which ingest then digest, fungi digest then ingest. Ingestion is the taking in of food or other substances. Digestion refers to the breakdown of food into smaller particles, capable of later absorbtion. Fungi produce exoenzymes to accomplish this. an enzyme that acts outside the cell which secretes it. most fungi store their food as glycogen (like animals)--plants store food as starch vegetative body may be unicellular (yeasts) or composed of microscopic threads called hyphae cell walls similar in structure to plants but differ in chemical composition--fungi cell walls are composed of mostly of chitin--plant cell walls are composed mostly of cellulose (plus lignin in secondary walls) cytoplasmic ultrastructure broadly similar to plants cells, but differ significantly in kinds of organelles and their structures. Structure of fungi The main body of most fungi is made up of fine, branching, usually colorless threads called hyphae. Each fungus will have vast numbers of these hyphae, all intertwining to make up a tangled web called the mycelium. The mycelium is generally too fine to be seen by the naked eye, except where the hyphae are very closely packed together. The picture on the left was taken through a microscope. The hyphae are magnified 100 times life size. In most molds, the hyphae contain cross walls called septa, which divide them into distinct uninucleate cell-like unit. These hyphae are called septate hyphae. In a few classes of fungi, the hyphae contain no septa and appear as long, continious cells with many nuclei. These are called coenocytic hyphea. The portion of a hypha that obtains nutrients is called the vegetative hypha; the portion concerned with reproduction is the reproductive or aerial hyphae, so named because it projects above the surface of the medium on which the fungus is growing. Types of fungi GILL FUNGI This type of fungus includes our familiar edible mushroom. Most, but not all gill fungi, have a stem bearing a cap on top. The gills, or lamellae as they are also known, are on the underside of the cap. The spores line the surface of the gills. A single fruiting body may produce as many as 10,000 million spores! The thickness of the gills, the way they are attached to the stem, and their spacing are all important ways of separating different species. There are in excess of 1,200 different species of gill fungi in Britain. Boletes These are fungi which have fruiting bodies similar to many of the gill mushrooms, in that they have a cap and a stem. However, boletes do not have gills on the undersurface of the cap. Instead, they have thousands of tiny tubes arranged perpendicular to the surface of the cap. The underside of the cap thus looks as if it is covered with thousands of little holes, or pores. Each hole is the end of one of the tiny cylinders, which is lined with spores. The fruiting bodies of some boletes in Britain reach sizes of 12" in diameter. Some tropical boletes may exceed 2 feet. Polypores Polypores tend to have very tough, leathery or woody fruiting bodies. They are often plate-like and most grow out of tree trunks or rotting wood, although some may grow on soil. Some of these fungi are known as Bracket Fungi, because they look like shelves growing out of the sides of trees. The pores are located on the underside of the fruiting body and as with the boletes, are lined with spores. Some of these fungi produce a new fruiting body every year, while others produce one which continues to grow year after year. Stinkhorn Stinkhorns are truly extraordinary fungi which grow out of a structure which resembles an egg. The fruiting body consists of a bell-shaped head mounted on a stalk. The head is covered in foul-smelling slime, which contains the spores. The

smell attracts flies which crawl around in the slime, becoming covered in spores. The flies disperse the spores when they leave and go elsewhere. Earthballs/ Puffballs and Earth Stars These fungi contain their spores inside a ball of some kind. The ball may be stalked or at ground level. The spore mass in the centre of the ball is solid to begin with, but later develops into a powdery mass of spores. In Earth Stars the ball has a tough outer covering which splits and spread out like petals to form a star-shape, exposing the inner spore-containing ball. The outer covering in Earth Balls just disintegrates with time to expose the inner spore mass, while in Puff Balls, the spores are released through a small pore at the top of the ball. Jelly Fungi This category includes a wide variety of fungi which produce fruiting bodies looking like shapeless blobs of jelly, or in shapes such as 'ears' and 'tongues'. They are soft, or jelly-like and can be found on trees, or on the ground Cup Fungi The cup fungi belong to an entirely different group of fungi to all of those described above. The scientific name for this group is 'Ascomycetes'. All of the fungi above belong to a group called 'Basidiomycetes'. The chief difference between these two major groups is in the method of producing spores. The Ascomycetes is a large group of fungi. They are the 'spore shooters'.

Chromoblastomycosis Chromoblastomycosis (also known as "Chromomycosis," "Cladosporiosis," "Fonseca's disease," "Pedroso's disease," "Phaeosporotrichosis," "Verrucous dermatitis") is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis). The infection occurs most commonly in tropical or subtropical climates, often in rural areas. It can be caused by many different type of fungi which become implanted under the skin, often by thorns or splinters. Chromoblastomycosis spreads very slowly; it is rarely fatal and usually has a good prognosis, but it can be very difficult to cure. There are several treatment options, including medication and surgery. Features The initial trauma causing the infection is often not noticed or forgotten. The infection builds at the site over a period of years, and a small red papule (skin elevation) appears. The lesion is usually not painful and there are few, if any symptoms. Patients rarely seek medical care at this point. Several complications may occur. Usually, the infection slowly spreads to the surrounding tissue while still remaining localized to the area around the original wound. However, sometimes the fungi may spread through the blood vessels or lymph vessels, producing metastatic lesions at distant sites. Another possibility is secondary infection with bacteria. This may lead to lymph stasis (obstruction of the lymph vessels) and elephantiasis. The nodules may become ulcerated, or multiple nodules may grow and coalesce, affecting a large area of a limb. Diagnosis The most informative test is to scrape the lesion and add potassium hydroxide (KOH), then examine under a microscope. (KOH scrapings are commonly used to examine fungal infections.) The pathognomonic finding is observing Medlar bodies, sclerotic cells. Scrapings from the lesion can also be cultured to identify the organism involved. Blood tests and imaging studies are not commonly used. On histology, chromoblastomycosis manifests as pigmented yeasts resembling "copper pennies." Special stains, such as periodic acid schiff and Gmri methenamine silver, can be used to demonstrate the fungal organisms if needed. Pathophysiology Chromoblastomycosis is believed to originate in minor trauma to the skin, usually from vegetative material such as thorns or splinters; this trauma implants fungi in the subcutaneous tissue. In many cases the patient will not notice or remember the initial trauma, as symptoms often do not appear for years. The fungi most commonly observed to cause chromoblastomycosis are:

Fonsecaea pedrosoi Phialophora verrucosa Cladosporium carrionii Fonsecaea compacta Over months to years, an erythematous papule appears at the site of inoculation. Although the mycosis slowly spreads, it usually remains localized to the skin and subcutaneous tissue. Hematogenous and/or lymphatic spread may occur. Multiple nodules may appear on the same limb, sometimes coalescing into a large plaque. Secondary bacterial infection may occur, sometimes inducing lymphatic obstruction. The central portion of the lesion may heal, producing a scar, or it may ulcerate.

Treatment Chromoblastomycosis is very difficult to cure. There are two primary treatments of choice.

Itraconazole, an antifungal azole, is given orally, with or without flucytosine (5-FC). Alternatively, cryosurgery with liquid nitrogen has also been shown to be effective.

Other treatment options are the antifungal drug terbinafine, an experimental drug posaconazole, and heat therapy. Antibiotics may be used to treat bacterial superinfections. Amphotericin B has also been used. Prognosis The prognosis for chromoblastomycosis is very good for small lesions. Severe cases are difficult to cure, although the prognosis is still quite good. The primary complications are ulceration, lymphedema, and secondary bacterial infection. There have been a few cases reported of malignant transformation to squamous cell carcinoma. Chromoblastomycosis is very rarely fatal. Prevention There is no known preventative measure aside from avoiding the traumatic inoculation of fungi. At least one study found a correlation between walking barefoot in endemic areas and occurrence of chromoblastomycosis on the foot. Epidemiology Chromoblastomycosis occurs around the world, but is most common in rural areas between approximately 30 N and 30 S latitude. Madagascar and Japan have the highest incidence. Over two thirds of patients are male, and usually between the ages of thirty and fifty. A correlation with HLA-A29 suggests that genetic factors may play a role as well. Chromoblastomycosis: Description: A mycotic infection of the cutaneous and subcutaneous tissues characterised by the development in tissue of dematiaceous (brown-pigmented), planate-dividing, rounded sclerotic bodies. Infections are caused by the traumatic implantation of fungal elements into the skin and are chronic, slowly progressive and localised. Tissue proliferation usually occurs around the area of inoculation producing crusted, verrucose, wart-like lesions. World-wide distribution but more common in bare footed populations living in tropical regions. Aetiological agents include various dematiaceous hyphomycetes associated with decaying vegetation or soil, especially Phialophora verrucosa, Fonsecaea pedrosoi, F. compacta and Cladophialophora carrionii. Clinical manifestations:

Lesions of chromoblastomycosis are most often found on exposed parts of the body and usually start a small scaly papules or nodules which are painless but may be itchy. Satellite lesions may gradually arise and as the disease develops rash-like areas enlarge and become raised irregular plaques that are often scaly or verrucose. In long standing infections, lesions may become tumorous and even cauliflower-like in appearance. Other prominent features include epithelial hyperplasia, fibrosis and microabscess formation in the epidermis. Chromoblastomycosis must be distinguished from other cutaneous fungal infections such as blastomycosis, lobomycosis, paracoccidioidomycosis and sporotrichosis. It may also mimic protothecosis, leishmaniasis, verrucose tuberculosis, certain leprous lesions and syphilis. Mycological and histopathological investigations are essential to confirm the diagnosis. Note: tissue hyperplasia forming a white verrucoid cutaneous lesion. In Australia, chromoblastomycosis due to C. carrionii occurs mostly on the hands and arms of timber and cattle workers in humid tropical forests. Laboratory diagnosis: 1. Clinical Material: Skin scrapings and/or biopsy. 2. Direct Microscopy: (a) Skin scrapings should be examined using 10% KOH and Parker ink or calcofluor white mounts; (b) Tissue sections should be stained using H&E, PAS digest, and Grocott's methenamine silver (GMS). Interpretation: The presence in tissue of brown pigmented, planate-dividing, rounded sclerotic bodies from a patient with supporting clinical symptoms should be considered significant. Remember direct microscopy or histopathology does not offer a specific identification of the causative agent. Note: direct microscopy of tissue is necessary to differentiate between chromoblastomycosis and phaeohyphomycosis where the tissue morphology of the causative organism is mycelial.

3. Culture: Clinical specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar. Interpretation: The dematiaceous hyphomycetes involved are well recognised as environmental fungi, therefore a positive culture from a non-sterile specimen, such as sputum or skin, needs to be supported by clinical history and direct microscopic evidence in order to be considered significant. Culture identification is the only reliable means of distinguishing these fungi. 4. Serology: There are currently no commercially available serological procedures for the diagnosis of chromoblastomycosis. 5. Identification: Culture characteristics and microscopic morphology are important, especially conidial morphology, the arrangement of conidia on the conidiogenous cell and the morphology of the conidiogenous cell. Cellotape flag and/or slide culture preparations are recommended. Causative agents: Cladophialophora carrionii, Fonsecaea pedrosoi, Phialophora verrucosa Management: The treatment of chromoblastomycosis has been exceedingly difficult. Successful surgical excision requires the removal of a margin of uninfected tissue to prevent local dissemination. Flucytosine with or without thiabendazole has been extensively used in the past. However both itraconazole [400 mg/day] and terbinafine [500 mg/ day] for 6 to 12 months have been used successfully for the treatment of chromoblastomycosis. Rhinocerebral mucormycosis Rhinocerebral mucormycosis is a rare opportunistic infection of the sinuses, nasal passages, oral cavity, and brain caused by saprophytic fungi. The infection can rapidly result in death. Rhinocerebral mucormycosis commonly affects individuals with diabetes and those in immunocompromised states. Rare variants of mucormycosis include lingual, pulmonary, cutaneous,

gastrointestinal (GI), and disseminated forms. The image below depicts a patient with rhinocerebral mucormycosis (see the images below). (See Etiology, Treatment, and Medications.) Most cases of mucormycosis are acute surgical emergencies; however, several cases of a more chronic, indolent form have been reported, with signs and symptoms developing over several weeks. Occurrence The pathogens that cause rhinocerebral mucormycosis are prevalent in nature but may be more prone to cause infection in moist, temperate climates. The exact frequency of rhinocerebral mucormycosis in the United States is unknown. Etiology Saprophytic aerobic fungi of the class Phycomycetes (order Mucorales) cause rhinocerebral mucormycosis, also known as phycomycosis. The 3 genera responsible for most cases are Rhizopus, Absidia, and Mucor. Researchers have also reported cases of rhinocerebral mucormycosis caused by Rhizomucor, Saksenaea, Apophysomyces, and Cunninghamella species. Phycomycetes are ubiquitous in nature, being commonly found in decaying vegetation, soil, and bread mold. They grow rapidly and can release large numbers of airborne spores. Thus, they are frequently found colonizing the oral mucosa, nose, paranasal sinuses, and throat. Phycomycetes do not generally cause disease in immunocompetent individuals who are able to generate phagocytic containment of the organisms. Persons at risk for infection (ie, immunocompromised individuals) typically also have decreased phagocytic activity because of an impaired glutathione pathway. In individuals who are immunocompromised, germination and hyphae formation occur, and this allows the organism to invade the patient's blood vessels. Mucormycosis is described almost exclusively in patients with compromised immune systems or metabolic abnormalities. Rhizopus species have an active ketone reductase system that enables them to thrive in an acidic pH and glucose-rich medium. Hyperglycemia enhances fungal growth and impairs neutrophil chemotaxis; therefore, individuals with diabetic ketoacidosis are commonly affected. Rhizopus species also favor an iron-rich environment and are frequently isolated in patients receiving deferoxamine therapy (an iron-chelating agent). In most cases, the fungi gain entry to the body via inhalation of airborne spores through the sinuses. It has been postulated that the most common reservoir for organisms is the pterygopalatine fossa. Infection spreads along vascular and neuronal structures and infiltrates the walls of blood vessels. Infections can erode bone through walls of the sinus and can spread into the orbit and the retro-orbital area, thereby extending into the brain. Invasion of nerves, blood vessels, cartilage, bone, and meninges, as well as perineural spread, are common. Direct invasion by fungal elements results in thrombosis and nerve dysfunction. Advancing infection can result in thromboses arising in the [4, 5, 6] cavernous sinus, carotid arteries, and jugular vein. Carotid artery occlusion has also been reported as a complication. Risk factors Seventy percent of mucormycosis cases occur in patients with diabetes mellitus, although this percentage is declining with the use of chemotherapy and with increasing frequency of various types of immunocompromised states. An underlying risk factor is recognized in more than 96% of mucormycosis cases. Risk factors for rhinocerebral mucormycosis include the following:
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Diabetes mellitus, Diabetes mellitus is a condition in which the pancreas no longer produces enough insulin or cells stop responding to the insulin that is produced, so that glucose in the blood cannot be absorbed into the cells of the body. Hyperglycemia, condition characterized by excessively high levels of glucose in the blood, and occurs when the body does not have enough insulin or cannot use the insulin it does have to turn glucose into energy. Iron overload Burns Human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS)

Blood dyscrasias, the pathologic conditions or disorders such as leukemia or hemophilia in which the constituents of the blood are abnormal or are present in abnormal quantity. Transplantation Immunosuppression (ie, prednisone therapy) Chemotherapy Intravenous drug use - Embolic to brain Disease states treated with high-dose steroids

This condition is a risk factor, particularly in association with poor glycemic control and acidosis, as it relates to cellular immune dysfunction. Patients with diabetes are predisposed to mucormycosis because of the decreased ability of their neutrophils to phagocytize and adhere to endothelial walls. Furthermore, the acidosis and hyperglycemia provide an excellent environment for the fungus to grow. (See the image below.) This diabetic patient with mucormycosis presented with complete ophthalmoplegia and proptosis. Note the complete ptosis and periorbital edema on the right side. Iron overload Iron overload states, as observed with hemochromatosis and deferoxamine treatment in patients receiving dialysis, may be risk factors. Iron enhances fungal growth and increases susceptibility. Researchers have reported infection in patients with liver and [7] renal failure. Burns In individuals with burns, mucormycosis generally involves only the skin and rarely results in rhinocerebral infection. Blood dyscrasias These include lymphoma, prolonged neutropenia, and leukemia. Researchers estimate that the incidence of mucormycosis in persons with hematologic malignancy is approximately 1%. Transplantation This includes solid organ (eg, liver, kidney) and bone marrow transplantation. Maertens et al found that the incidence of mucormycosis in recipients of allogeneic bone marrow transplants was 1.9%. However, most cases do not involve the central nervous system (CNS). Graft versus host disease (GVHD) and donor leukocyte infusions are also risk factors. Disease states treated with high-dose steroids One case report described mucormycosis in a patient with an adrenal corticotropic hormone (ACTH)producing pulmonary tumor associated with Cushing syndrome. Prognosis Rhinocerebral mucormycosis carries a prognosis of high morbidity and mortality. Survival depends on the reversibility of underlying risk factors and early surgical intervention. Complications Rhinocerebral mucormycosis progresses rapidly and can result in carotid artery occlusion, cavernous sinus thrombosis, and CNS infarction secondary to fungal thrombosis, leading to hemiparesis, hemiplegia, coma, and death. Other complications of
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rhinocerebral mucormycosis include CNS hemorrhage, abscess, and cerebritis, as well as blindness and airway obstruction from head and neck infections. Permanent residual effects of the disease occur up to 70% of the time. Neurologic function can be recovered if no irreversible damage has occurred, but morbidity is very common. Postsurgical disfigurement is likely. Mortality No survivors of mucormycosis were reported before 1955. (Amphotericin became available in the 1950s.) Mucormycosis has a fulminantly fatal clinical pattern. The survival rates among patients with invasive sinus disease without cerebral involvement may be as high as 50-80%. If infection spreads to the brain, the case fatality rate can exceed 80%. Death may occur within 2 weeks if mucormycosis is not treated or is unsuccessfully treated. The prognosis of mucormycosis may improve with rapid diagnosis; early management, including combined antifungal and surgical interventions; and reversal of underlying risk factors. One case series reported a survival rate of approximately 80% when both medical and surgical interventions were administered. The cause of death in many patients is mucormycosis itself rather than the progression of the underlying disease. The mortality rate in diabetic patients appears to be lower than in nondiabetic patients and in patients with intracerebral involvement. Patients who have been treated with amphotericin B and who have had orbital exenterations are more likely to survive. Patients with frontal sinus involvement and older patients have lower rates of survival. A meta-analysis by Yohai et al indicated that the survival rate declines when interval from diagnosis to treatment is longer than 6 days.