A mold capable of growing and spreading even at colder temperatures. It is both an allergenic and a toxigenic type of mold that grows in homes with water damage. Typically, fusarium will grow in carpeting, wallpaper and other fabrics and materials. Fusarium mold is often pink, white or reddish in color and naturally grows on food products and in compost. Exposure to fusarium can cause skin infections as well as allergic reactions symptoms such as sore throat, running nose, sneezing, itchy eyes and dermatitis. Prolonged exposure to fusarium can cause other sever and life-threatening conditions such as bone infections or a brain abscess. Fusarium can produce toxins that are damaging to the nervous system and can potentially lead to hemorrhages and internal bleeding. By nature, it will quickly spread from room to room. If you notice it in one area of your home, examine the rest of the home thoroughly for signs of it elsewhere.
Fusarium is listed as one capable of causing mycetomas, and it has repeatedly been isolated from human keratitis and corneal ulcers. Most cases concern keratitis. It has been reported as an agent in endophthalmitis, subcutaneous and cutaneous infections, septic arthritis and mycetoma. Cases of sinusitis and catheter infection have been reported. Upon initial exposure, Fusarium generally ascends right into the colon, then through the tissues and through the central nervous system.
Although they are not the most toxic of all types of fusarium mycotoxins, fumonisins (Fm) and DON are the most frequently detected and, therefore, most often associated with illness in farm animals or humans. Fumonisins cause a neurological disease, equine leucoencephalomalacia in horses, pulmonary edema in swine, hepatotoxic and nephrotoxic effects in other domestic animals, and carcinogenesis in laboratory animals. The American Association of Veterinary Laboratory Diagnosticians has recommended maximum levels of 5, 10, and 50 ppm fumonisin B1 (the most commonly detected of more than 11 structurally related fumonisins) in feed for horses, swine, and beef and poultry, respectively.
Although relatively high levels of fumonisins have been detected in corn in some areas of the world with high rates of esophageal cancer in humans, it has not been determined whether fumonisins are causally related to development of this cancer. A recent report from India described an acute but self-limiting food borne disease outbreak in villagers consuming moldy corn containing up to 64. 7 mg fumonisins/kg. It is not known whether lower mycotoxin concentrations, chronically consumed, cause other detrimental effects in humans, and tolerance levels for fumonisins have not been set for fumonisins in grains for human consumption (with the exception of Switzerland, which has set a level of 1 ppm). The trichothecenes fusarium can produce are potent inhibitors of DNA, RNA, and protein synthesis, and have been well studied in animal models because of concern about their potential misuse as agents of biological warfare, due to their ability to destroy human health, alter DNA, and affect the mind.
The first recognized tricothecene mycotoxicosis was alimentary toxic aleukia in the USSR in 1932; the mortality rate was 60%. In regions where the disease occurred, 540% of grain samples cultured showed the presence of Fusarium sporotrichoides, while in those regions where the disease was absent this fungus was found in only 2-8% of samples.
DON is sometimes called vomitoxin because of its toxic effects on swine and other animals. Humans consuming flour made from scabby wheat or moldy corn containing DON also have been reported to suffer nausea and headaches which lasted 2-4 days. DON is frequently present at high concentrations (usually >1 ppm, sometimes as high as 20 ppm) in wheat and corn. Although no U. S. government regulation has been made regarding levels of Fusarium toxins in human foods or cigarettes, a recommended tolerance level of 1 ppm DON in grains for human use has been set by several countries, including the USA, while higher concentrations are permitted in animal feeds. See chemical breakdown and health implications below.
Morphology: Colonies around 8. 5 – 9. 5 cm in diameter after 7 days on PDA, cottony, yellow, reddish, red-brown or red-purple with whitish aerial mycelium overlaid. Conidiophores branching, bearing phialides which often make fork-like proliferations at the tip as new secondary phialidic necks are produced. Micro conidia ranging from subglobose and 5 – 7 ?m in diameter to pear or spindle shaped, mostly 6 – 11 X 3 – 4 mm, usually unicellular, sometimes bicellular. Macro conidia slightly curved, 3 – 5 septate, thin, 30 – 45 X 3. 5 – 5. 5. ?m. Chlamydospores abundant, yellow-brown, usually in chains.
- Trichothecenes: a variety, most prominently T-2 toxin, HT-2 toxin, neosolaniol and fusarenon-X. These are strongly toxic compounds. Like the macrocyclic trichothecenes mentioned above, their primary toxic mechanism is the inhibition of protein synthesis at the level of the ribosome. For the most part, their effects are known from instances in which humans or animals ate contaminated grain, or from laboratory animal or in vitro studies. The major effects observed include “vomiting; inflammation; diarrhea; cellular damage of the bone marrow, thymus, spleen and mucous membranes of the intestines; and depression of circulating white blood cells. ” Humans who have eaten contaminated grain develop “alimentary toxic aleukia,” which begins with burning sensations of the mouth, throat, esophagus and stomach, continues with vomiting, diarrhea and gastric cramps, and finally progresses to severe leukopenia (drop in white blood cell count), which renders the patient susceptible to infections. Death may result. Skin contact with material laden with these trichothecenes induces contact dermatitis, and in stronger exposures lesions may be necrotizing (that is, may contain dead tissue, a significant risk factor for the development of bacterial infections). Effects on immune system components apart from the above-mentioned killing of thymus and spleen cells include inhibition of lymphocyte proliferation responses (e. g., mitogen response) and disruption and lysis of alveolar macrophages. Coagulation factors in the blood (except fibrinogen) are also significantly depressed. Trichothecenes in general seem to have little carcinogenicity, but when consumed or administered in pregnancy may have some teratogenicity (inducing deformed offspring) or abortifacient properties.
- Zearalenone: a few isolates of F. sporotrichoides have been verified as producing this toxin. This compound is an estrogen mimic, most commonly causing vulvovaginitis (swelling and reddening of the vulva) in gilts (young female pigs) and sows which have consumed contaminated feed. This condition sometimes leads to vaginal or rectal prolapse.common results include reduced litter size, loss of pregnancy, and poor milk production in affected swine. Males may be feminized to some extent. Similar syndromes occur in cattle and sheep fed zearalenone-contaminated grain.
Morphology: colonies are very rapidly growing, exceeding 9 cm after 7 days on PDA, aerial mycelium whitish to yellow or tan, substrate mycelium and reverse carmine to intensely red brown. According to Domsch et al., the aerial mycelium is very hydrophobic (difficult to wet), unlike that of the similar species F. graminearum. Phialides are monophialides: that is, they do not proliferate at the tips to form multiple fertile necks. Microconidia are absent. Macroconidia are distinctly stout, mostly 5-septate and 30 – 50 X 5 – 7. 5 ?m. Chlamydospores are abundant, brownish, in chains or in clumps.
The species can be distinguished with some difficulty from the similar F. graminearum and F. crookwellense. F. graminearum has macroconidia with relatively parallel dorsal and ventral sides, while the “back” of the F. culmorum macroconidium is strongly bowed or arched. The catch is that this character is best seen on carnation leaf agar, a medium usually only used by the most specialized fusariologists. In addition, isolates in good condition (i. e., isolates either freshly obtained from nature or retaining the characters of freshly isolated cultures) of F. culmorum, on PDA, often conidiate abundantly around the point of inoculation, while F. graminearum in good condition does not do so. The condition is mentioned because Fusarium species frequently deteriorate after a few subcultures, and slimy, profusely macroconidial (pionnotal) colonies are one type of degeneration seen. Such degenerate isolates produce masses of conidia all over the colony surface, regardless of which species they belong to.
F. crookwellense tends to have the same conidiation at the point of inoculation that F. culmorum has. It also has macroconidia with relatively strongly curved dorsa, compared to those of F. graminearum, just as F. culmorum does. According to Burgess et al. “the macroconidia (of F. crookwellense) are longer and not as wide as those of F. culmorum. . . (and) in contrast to the conspicuous foot at the end of the basal cell of an F. crookwellense macroconidium, that of F. culmorum is less obvious. ” A comparison of the photos published by Nelson et al. makes this more clear than descriptive text does.
- Trichothecenes: The major compound produced is deoxynivalenol (vomitoxin). This toxin is somewhat less toxic than the compounds listed for F. sporotrichoides, above, but causes a serious feed refusal and emesis (vomiting) syndrome in animals fed contaminated feed, especially pigs.
Colonies fast growing, exceeding 9 cm after 7 days on PDA, with white to pink aerial mycelium and red agar surface and reverse, and with a distinct odour suggesting peaches. Phialides are monophialides, short (6 – 18 ?m) and blunt, in clusters. Microconidia predominantly globose to broadly pyriform, with a basal apiculus, 6 – 10 X 5. 5 – 7. 5 ?m. Macroconidia relatively sparse, 2 – 3 septate, 18 – 38 X 3. 8 – 7. 0 ?m, occasionally longer and with up to 5 septa. Well defined chlamydospores not present, but there are some thickened portions of hyphae which are reminiscent of chlamydospores.
- Trichothecenes: Although a variety of trichothecenes have been attributed to this species in the past, the careful reassessment of Marasas et al. found only diacetoxyscirpenol produced in significant quantity by a large number of cultures. This compound is slightly less toxic than T-2 toxin, but in general has effects similar to those described for the toxins of F. porotrichoides, above. F. poae has been held by some scientists in the former Soviet Union to be particularly involved with bone deformity in animals and people who have eaten contaminated material. The identification, however, of the isolates used to draw these conclusions needs to be re-investigated before this attribution can be confirmed. A human disease, Kashin-Beck disease, has been described based on characteristic bone deformities seen in populations in affected areas. Although F. poae contamination has been proposed as etiologic in this disease, other theories have also been put forward and the final resolution of the matter is not clear.
Fusarium equiseti (sexual state Gibberella intricans)
Colonies 7 – 8 cm after 7 days on PDA, yellowish, ochre or buff finally becoming yellow-brown to brown, but never red. Phialides are monophialides, often in densely branching penicillate tufts. Microconidia absent. Macroconidia usually distinguished by extension of the apical cell into a pronounced beak; either nearly straight or strongly curved, 3 – 5 septate, with basal cell extended as a distinct pedicel, 30 – 50 (-65) X 4. 0 – 5. 0 ?m. Chlamydospores abundantly produced, in chains.
- Most commonly diacetoxyscirpenol (see F. poae), and in at least some strains also T-2 toxin, fusarenon-X and neosolaniol (see F sporotrichoides) are produced.
Morphology: Colony reverse usually pale purple; microconidia club-shaped with flat (truncate) basal end, seen in a 10X observation of undisturbed colony on low-sugar media to be formed all or partly in chains rather than slimy heads, phialides mostly under 30 ?m, not proliferating (forking) at the tips. Chlamydospores not found.
- Fumonisins: These toxins were first described in 1984 after a concerted search for the cause of equine leukoencephalomalacia, a disease of horses in which brain tissue is damaged and horses show ataxia (inability to coordinate walking), facial and other paralysis, partial blindness, lethargy or excitement, and in later stages lameness, inability to stand, seizures and death. After the purification of fumonisins, the disease was induced in horses with purified material, confirming the etiologic role of the mycotoxin. Liquefactive necrosis of white matter areas of brain tissue is the main pathological sign seen. Hepatotoxicity is also seen. Experimental animals often experience hepatotoxicity, nephrotoxicity or both; rats have also been shown to experience necrosis of stomach mucosa and myocardium. Liver cancers are induced. Fumonisins are also among the chief suspects for the agent(s) of elevated levels of esophageal cancer in certain parts of the world.
Morphology: much like F. moniliforme but older phialides proliferate (fork) extensively near the apex. Proliferating phialides can be very difficult to find in colonies younger than 7 days. Chlamydospores not found.
Toxins: fumonisins (see F. moniliforme)
Morphology: Colony reverse usually purple or pale; microconidia ellipsoidal, sometimes curved, produced in slimy heads not chains, phialides producing microconidia are mostly under 20 ?m, often quite short and broad, not proliferating (forking) at the tips. Macroconidia rather sharply pointed and hooked over at the apex. Chlamydospores often found, seldom abundant.
Toxins: the picture of which toxins may be produced by the majority of F. oxysporum isolates is unclear and questionable.
Morphology: Colony reverse usually pale tea-brown or pale, sometimes reddish-brown to purplish (especially on cycloheximide medium); microconidia ellipsoidal, macroconidia with ends more blunt than those of other species (but don’t rely on this character alone); phialides producing microconidia are thin and elongate, often 20 – 40 mm long (best single character to look for to distinguish from F. oxysporum), not proliferating (forking) at the tips; chlamydospores often abundant, rough.
- Naphthaquinone pigments. These pigments are not currently regarded to be mycotoxins significantly affecting humans or animals.
Fusariosis in Humans: Fusarium-Infected Humans
Human Fusarium infection or Fusariosis, usually occurs in immunocompromised individuals, such as those affected by other diseases such as AIDS (HIV) or even a case of the common cold. Extreme exhaustion can also produce an immunocompromised state. Fusarium attacks cells in humans much the way in attacks cells in plants -through the secretion of mycotoxins that it itself is immune to. These mycotoxins dissolve the cell walls, and the fungus is then free to absorb the cell’s contents, and enter the cell cavity, reproduce, and continue the process attacking other cells.
The first reference we have to Fusarium in humans dates from an 1916 article published in French by Dr. N. V. Greco in an Argentine Medical Journal called Origine des Tumeurs (Etiologie du Cancer, etc. ) et Observations de Mycoses (Blastomycosis, etc) Argentines in which he described a fungal infection of the nose which he believed to be caused by a Fusaria.
“Members of the genus Fusarium are ubiquitous fungi uncommonly associated with infection. Human infection sometimes occurs as a result of inoculation of the organism through the body surface, thus causing skin infection, onychomycosis, keratitis, endophthalmitis and arthritis. Fusarium is one of the fungi that can produce micetoma. Dissemination may occur in subjects with underlying immunodeficiency.
Disseminated fusariosis typically occurs in neutropenic hosts and carries a high mortality rate. Characteristically, a profoundly neutropenic patient has had the abrupt onset of fever, sometimes with myalgia, followed in 66 percent of cases by distinctive skin lesions: multiple sites, predominantly on the extremities, develop painful erythematous macules or papules. Central pallor is followed by necrosis and ulceration. Blood cultures have been positive in 59 percent of cases, including a few that seemed to be due to infected central venous catheters. Amphotericin B is the drug of choice, although it appears to be poor correlation between in vitro susceptibility and clinical response. Prognosis is poor, with a mortality of 76% in the 85 reported cases. Survival was related to the resolution of the neutropenia. ” From Washington University Infectious Diseases Division Fusarium handouts.
“The genus Fusarium contains important mycotoxin-producing species that have been implicated in human diseases, such as alimentary toxic aleukia, Urov or Kashin-Beck disease, Akakabi-byo or scabby grain intoxication, and esophageal cancer. Many of these mycotoxin-producing species have also been implicated in several animal diseases, including hemorrhagic, estrogenic, emetic, and feed refusal syndromes, fescue foot, degnala disease, moldy sweet potato toxicosis, bean hulls poisoning, and equine leukoencephalomalacia.
The interest in toxigenic Fusarium species is increasing world-wide due to the discovery of a growing number of naturally occurring Fusarium mycotoxins that have practical importance as threats to human and animal health. “quoted from Toxigenic Fusarium Species by Marasas et alia, Penn State U, 1984. It is also fast becoming a worldwide problem related to sick buildings.
Chemical Breakdowns of Fusarium Mycotoxins
- 4-Acetoxyscirpenediol= 4$-3-acetoxy-3″, 15-dihydroxy-12,13-epoxytrichothec-9-ene.
- A similar compound, monodeacetylanguidin = 4- or 15-acetylscirpentriol.
- 3-Acetyldeoxynivalenol(= Deoxynivalenol monoacetate) = 3″-acetoxy-7″,15-dihydroxy-12,13-epoxytrichothec-9-en-8-one 8-Acetylneosolaniol(= Neosolaniol monoacetate) = 4$,8″, 1 5-triacetoxy-3″-hydroxy-1 2,13-epoxytrichothec-9-ene 4- or 15-Acetylscirpentriol.
- See 4-Acetoxyscirpenediol Acetyl T-2 toxin= 3″,4$,15-triacetoxy-8″-(3-methylbutyry(oxy)-1 2,1 3-epoxytricho-thec-9-ene Anguidin. See Diacetoxyscirpenol.
- Avenacein +1Beauvericin +2 Butenolide= 4-acetamido-4-hydroxy-2-butenoic-acid -(-lactone.
- Calonectrin= 3″, 1 5-diacetoxy-12,13-epoxytrichothec-9-ene.
- 15-Deacetylcalonectrin(= 1 5-De-0-acetylcalonectrin) = 3″-acetoxy-1 5-hydroxy-12,13-epoxytrichothec-9-ene.
- Deoxynivalenol (= Rd toxin, = Vomitoxin) = 3″,7″,15-trihydroxy-12,13-epoxytricho-thec-9-en-8-one Deoxynivalenoldiacetate. See Diacetyldeoxynivalenol Deoxynivalenol monoacetate. See 3-Acetyldeoxynjvalenol DiacetoxyscirpendiolSee 7″-Hydroxydiacetoxyscirpenol Diacetoxyscirpenol(= Anguidin) = 4$,15-diacetoxy-3″-hydroxy12,13-epoxytrjchothec-9-ene.
- DiacetoxyscerpentriolSee 7″,8″-Dihydroxydiacetoxyscirpenol Diacetyldeoxynivalenol(= Deoxynivalenol diacetate) = 3″,15-diacetoxy-7-hydroxy 12,13-epoxytrichothec-9-en-8-one.
- Diacetylnivalenol (= Nivalenol diacetate) = 4$,15-diacetoxy-3″,7″-dihydroxy-12,13-epoxytrichothec-9-en-8-one 7″,8″-Dihydroxydiacetoxyscirpenol (= Diacetoxyscirpentriol) = 4$,15-diacetoxy-3″,7″,8″-trihydroxy-12,13-epoxytrichothec-9-ene Enniatins +1 Fructigenin +1 Fumonisin B1 1 1,2,3-propanetricarboxylic acid 1,-l-[1-(12-amino-4,9,11-trihydroxy-2-methyltridecyl)-2-(1-methylpentyl) -1,2-ethanediyl] ester; macrofusine + Fusarenon. See Fusarenon-X.>
- Fusarenon-X(=Fusarenon, = Monoacetylnivalenol, = Nivalenol monoacetate) = 4$-acet oxy-3″,7″, 15-trihydroxy-12,13-epoxytrichothec9en8one Fusaric acid (= Fusarinic acid) = 5-butylpicolinic acid.
- Fusarinic acid.
- F-See Zearalenone HT-2 toxin= l5-acetoxy-3″,4$-dihydroxy-8″-(3-methylbutyryloxy)-12$-epoxytricho-thec-9-ene.
- 7″-Hydroxydiacetoxyscirpenol(= Diacetoxyscirpendiol) = 4$,15-diacetoxy-3″,7″-dihydroxy-12,13-epoxytrichothec-9ene 8″-HydroxydiacetoxyscirpenolSee Neosolaniol.
- 1,4-Ipomeadiol= 1-(3-furyI)-1 ,4-pentanediol Ipomeanine= 1-(3-furyl)-1 ,4-pentanetione.
- 1-Ipomeanol= 1-(3-furyl)-1-hydroxy-4-pentanone 4-lpomeanol= l-(3-furyl)-4-hydroxy4pentanone Lateritin +1 Lycomarasmin +1 Moniliformin= potassium or sodium salt of 1-hydroxycyclobut-1-ene-3,4-dione Monoacetoxyscirpenol= 15-acetoxy-3″,4$~djhydroxy-12,13-epoxytrichothec-9ene MonoacetylnivalenolSee Fusarenon-X Monodeacetylanguidin.
- See 4-Acetoxyscirpenediol Neosolaniol(= 8″-Hydroxydiacetoxyscirpenol) = 4$,15-diacetoxy-3″8″-dihydroxy 12,13-epoxytrichothec-9-ene NeosolaniolacetateSee 8-Acetylneosolaniol Neosolaniol monoacetate.
- See 8-Acetylneosolaniol Nivalenol= 3″,4$,7″, 15-tetrahydroxy-12,13-epoxytrichothec-9-en-8-one Nivalenol diacetateSee Diacetylnivalenol Nivalenol monoacetateSee Fusarenon-X NT-1 toxin(=T-1 toxin) = 4$, 8″-diacetoxy-3″,15-dihydroxy-12,13-epoxytrichothec-9-ene NT-2 toxin= 4$-acetoxy-3″, 8″, 1 5-trihydroxy-1 2,1 3-epoxytrichothec-9-ene Rd toxin See Deoxynivalenol Sambucynin +1Scirpentriol = 3″,4$, 1 5-trihydroxy-12,13-epoxytrichothec-9-ene SolaniolSee Neosolaniol T-1 toxinSee NT-1 toxin T-2 toxin = 4$,15-diacetoxy-3″-hydroxy-8″-(3-methylbutyrlyloxy)-12,13-epoxytrichothec-9-ene Triacetoxyscirpendiol= 4$,8″,15-triacetoxy-3″,7″-dihydroxy-1 2,1 3-epoxytrichothec-9-ene Triacetoxyscirpenol= 3″, 4$,15-triacetoxy-12,13-epoxytrichothec-9-ene Vomitoxin See Deoxynivalenol Yavanicin+1 Zearalenol= 2,4-dihydroxy-6-(6, 1O-dihydroxy-trans-1 -undecenyl)-benzoic acid :-lactone Zearalenone= 6-(10-hydroxy-6-oxo-trans-1-undecenyl)-$-resorcylic acid lactone