11th lecture Fungal diseases Flashcards
Fungal diseases
- Not transmissible diseases
- Invade organs (invasive fungi)
- Produce toxins (mycotoxicosis)
- Most important:
- aspergillosis (respiratory tract)
- candidiasis (digestive tract)
- ochrochonosis (encephalitis)
- zygomycoses (Mucor, Rhizopus, Absidia)
- histoplasmosis, cryptococcosis (rare, but risk for humans)
Aspergillosis - pneumomycosis
-Aspergillus fumigatus (A. flavus, niger, glaucus, terreus)
• soil saprophytes grow in warm, humid environment
• In embryonated egg, air cell, litter, feed, ventillation system
• Infection with inhalation of spores (conidia)
-Affects the lower respiratory tract:
• pneumonia caused by moulds, pneumomycosis
• mycotic pneumonia
• Sometimes also: eye, brain, skin, joint & viscera
• Systemic infection can also occur
-Appearance:
• In young birds: acute form, high morbidity/mortality
• In adult birds: chronic form, economical loss
• poor management, cold, stress, ammonia &dust, overcrowding, immunosuppression
• all bird species are susceptible
• most often turkey and chicken
Pneumomycosis
Aspergillosis pathogenesis
• infection: aerogenous (inhalation)
• 2-3 µm spores – bypass the physical barrier of the airways
-pathogenesis:
• deposit in the parabronchial/air sac epithelia
• granuloma formation in the lumen of the parabronchi and in the lumes of the atria around the spores
• 1-9 mm white-yellow nodules, plaques
• disseminate via blood
• following multiple metastatis generalization occurs
• also produce immunodepressive & cytotoxic toxins
• proteolytic enzymes – degrade host tissue
Pneumomycosis
• Clinical signs:
-Hatchery contamination:
• 3-5 days PE: dyspnea, polypnea, open-mouth breathing, death
• Mortality rate: 5%-50% in the first 3 weeks
• Survivors: weak, showing chronic respiratory signs, lethargic, stunted
-In adult birds: subclinical infection, chronic respiratory signs
-metastasis: brain, eyes etc.
• ophtalmitis mycotica
• encephalitis mycotica
• Diagnosis:
• No pathognomic clinical signs (DD: other respiratory diseases)
• cultural isolation, identification
-Treatment:
• not attempted, affected birds should be culled
• prevention
Candidiasis Pathogen
-Mycosis (pseudohyphae formation) caused by a yeast,
thrush
• Oral, esophageal, crop candidiasis occurs frequently
• result of opportunistic infection
• concurrent disease, nutritional deficiency, immunosuppression
• altered flora post-AB therapy (!)
• lack of sanitation, heavy parasitism, vitamin deficiency, diet rich in CHs
-Pathogens:
• Candida albicans (most common)
• affects young birds, < 3 weeks of age
• chicken, turkey, guinea fowl, geese, pigeon, quail, peacock
• Aquired by ingestion, invades the superficial epithelial layers
• results in hyperplasia, pseudomembrane formation
-Clinical signs
• not specific (reduced growth, decrease in feed intake)
• lesions located in the crop (less in the proventriculus, esophagus,
mouth)• In the crop:
• coated with multiple or confluent mats (cannot be washed off)
• circumscribed or diffuse appearance
• easily removable greyish-white pseudomembrane layer, superficial necrotic inflammation (ulceration)
Candidiasis Diagnosis
- Diagnosis:
- pseudomembranes are highly suggestive
- Histologic examination of scrapings, culture
- DD: ingection of toxic products, mycotoxins, trichomoniasis
Treatment:
• Best prevented (by controlling predisposing factors)
• sanitation
Mycotoxicoses
-Ingestion of feed contaminated with toxins produced by fungi
• mycotoxins = (secondary) metabolic products of fungi
• In the feed industry mycotoxin levels are too low to cause acute
mycotoxicosis, but lower production performance occurs
• no treatment is available, need to prevent fungal growth
-Contamination:
• Before harvest (Fusarium)
• During storage (ochratoxin A): the mycoflora changes during storage
> xerophilic spp release water, hydrophilic species use it
- fungi produce mycotoxins only under special environmental
circumstances
• humidity, temperature
• some fungi produce different mycotoxins under different environmental
circumstances
• mycotoxins are stable in feed, resistant to conventional thermal treatments
• synergistic or additive effect!
-General consequences
• change in appearance, organoleptic qualities, technological properties
• decrease in nutritional value
-fungi are present almost everywhere in the environment• hundreds are identified, but around 30 have real importance
-their metabolic products may be expected everywhere
• in forage of vegetal/ animal origin
• the mycotoxins have different target organs
• some mycotoxins can be harmful for several organs
• some mycotoxins can have general effect
• some mycotoxins highly impair
• the GI tract
• the liver
• the kidney
• the bone marrow
• the immune organs
• the nervous system
Aflatoxicosis
- Ingestion of feed containing aflatoxin (AFB1)
- produced by Aspergillus flavus, A. parasiticus
- Cummulative effect! Hepatotoxic & immunosuppressive effect
-Clinical signs vary
• according to species, age, quantity, duration of exposure
• young birds (and males) are more susceptible
-Acute intoxication (duck, turkey)• several mg/kg
• apathy, ruffled feathers, diarrhea, ataxia, convulsions, death
• hepatomegaly with necrotic-hemorrhagic foci
• enlargement of kidney, spleen, pancreas, atrophy of bursa
-Chronic intoxication
• Exposure for several weeks
• Fatigue, anorexia, low production performance
• Drop in egg production, reduced growth rate
• hepatocyte necrosis, regeneration, bile duct cell proliferation
Ochratoxicosis
- Ochratoxin A
- Produced by Aspergillus ochraceus, Penicillium groups
-Nephrotoxic
• severe renal failure and uraemia in all avian species
• regression of bursa and thymus (immunosuppression)
• Mortality can go up to 50%
-Clinical signs:
• Acute form: asthenia, ataxia, tremors, impaired
reflexes
• 2-10 mg/kg
• Chronic form: reduced growth rate, poor FCR
Trichothecene toxicosis
- Production: by Fusarium species
- before harvest in the field
- most intensive: in humid environment, 4-24°C
- Some are highly toxic• T-2
-Clinical signs:
• asthenia, inappetence, diarrhea, panting, reduced weight gain
-local effect:
• irritation & necrosis of skin, oral& GI mucosa hemorrhages
• Liver cell necrosis
- general effect: cytotoxic effect
• growth retardation, feathering abnormalities
• drop in egg production, decreased hatchability
• immunosuppression
Fumonisin toxicosis
- Production: by Fusarium species
- discovery in late 80’s
- around harvest period when outdoor conditions are mild & humid
- several hundreds mg/kg needed
- Fumonisin B1: most frequent and toxic
- ducks are the most sensitive
- increase in mortality,
- economic loss due to impact on the quality of foie gras
- Clinical signs:
- poor FCR, growth retardation
Other mycotoxicoses
-Cyclopiazonic acid (CPA) toxicosis
• produced by Aspergillus and Penicillium species
• reduction of weigth gain, ataxia, apathy, spasms
• proventricular dilatation syndrome of broiler chickens
-Citrinin
• produced by Aspergillus and Penicillium species
• degeneration and necosis of tubular epithelial cells
- Zearalenone
• Estrogenic effect
• Birds are resistant, turkeys are most sensitive
• testicular dystrophy and atrophy in male goose, turkey, guinea-fowl
-Fusarochromanone toxicosis
• dyschondroplasia in broiler chickens, breast blisters
• economical loss due to carcass downgrading
• negative effect on hatchability
Intestinal coccidiosis
protozoan parasites, belong to Eimeriidae
• huge economical impact (widespead use of prophylactic medications)
• obligate IC parasitic protozoa
• All chicken coccidian are
species-specific (occur only in the chicken)& tissue tropic (occur in particular areas of the intestine)
-Replication: 7 phases,
• Once ingested & released there are 2 cycles of asexual reproduction
(schizogony) and 1 cycle of sexual reproduction (gametogony)
• Stages of coccidia in chickens appear both within the host & outside.
• The oocyst contains 8 bodies (sporozoites)
• the developmental stages in the chicken give rise to a oocyst• microscopic egg, that is passed out in the droppings
• the oocyst develops within 1-2 days to form a sporulated
oocyst=>capable of infecting other chickens
• contain 4 sporocysts, each sporocyst 2 sporozoites
Coccidiosis in chicken
Pathogen: Eimeria ssp.
- E. acervulina – in the first part of the SI
- E. necatrix, E. mitis, E. maxima – middle part of SI
- E. brunetti –colorectum
- E. tenella – caecum
- either schizogony, or gametogony
- take places in that part of the intestine which is proper for the pathogen, the proliferation results in cell destruction
- The severity of the lesions is judged according to the extent &depth of the cell loss
Lesion scoring
Quantitative macroscopic system
From „0” to „4”
• From mild to severe
• Based on hemorrhages, greyish-white foci, tickness of the wall
• Content and dilatation of the intestines
