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
Coccidiosis in chicken
- Acute catarrhal enteritis
- Fibrinous enteritis
- croupous, diphteric
- Hemorrhagic enteritis
- Ulcerative enteritis
- Necrotic enteritis
- Chronic enteritis
Cryptosporidiosis
• Protozoa:Cryptosporidium
• C. baileyi (intestine, airways), C. meleagridis (intestines)
• primary pathogens in chicken, turkey and quails
• Life cycle: 2 types of oocysts
• Thick-walled oocysts: infect the host
• Thin-walled: responsible for endogenous self-infections
• No organ specificity
• Immune status & intercurrent diseases have an effect
on distribution
• Age-related non-specific and specific immunity
• Young birds are more susceptible
• Marek disease, IBD inhibit immunity chronic shedding
Cryptosporidiosis Forms
- Reported worldwide
- Inhalation or ingestion of oocysts (100 are enough)
- Invasion of the cloaca, bursa and respiratory tract
- Rapid spreading in the flock (direct contact)
- Vectors: wild birds, rodents, insects
-Respiratory form
• Sinusitis, upper/lower respiratory tract infection
• Growth retardation, elevated premature mortality
-Gastrointestinal form
• Affects whole GI tract & bursa
• Watery diarrhea, growth retardation
-Renal form (rare)
• No clinical signs; Kidney: enlarged, pale, white foci
Cryptosporidiosis
• Diagnosis:
-Diagnosis:
• No specific clinical signs
• Histology, scrapings, direct detection, antigen detection
• Serology, PCR
-Treatment: • No effective product • Biosecurity measures • Disinfectants • Steam cleaners (>35°C)
Histomoniasis (histomonosis)
„Blackhead disease” (cyanosis of the head)
• Head carried low
-Parasitic typhlohepatitis of turkeys
• Acute form: sulphur-yellow diarrhea, death
• caseonecrotic lesions in the liver and ceca
• Other species can be infected as well
-Pathogen: flagellated protozoan
• Histomonas meleagridis
• Amoeboid form: lacking flagellum found in tissues
• Flagellated form: in the lumen of the ceca
• Life cycle is linked to Heterakis gallinarum
• Ingestion of the nematode’s egg contaminated with Histomonas
• Multiplication in the lumen of the ceca
• Hematogen spread to the liver through the cecal wall
Infectious enterohepatitis of turkey
(Histomonosis)
Pathogenesis
• Susceptible:• Young poult, chicken, guinea fowl, peacock, pheasant
-Pathogen: Histomonas meleagridis
• pleomorphic protozoan
• exists in dimorphic forms
• amoeboid (in tissues) and flagellated (in cecal lumen)
• present in the environment of the turkey
-Infection:
• transmitted most often in embryonated eggs of the cecal nematode Heterakis
gallinarum
• The primary lesions are in the ceca, which exhibit marked inflammatory changes &
ulcerations, causing a thickening of the cecal wall
-pathogenesis:
• Histomonads are released from Heterakis larvae in the ceca a few days after entry of the nematode & replicate rapidly in cecal tissues
• the parasites migrate into the submucosa & muscularis mucosae => cause extensive and severe necrosis
• Histomonads reach the liver either by the vascular system or via the peritoneal cavity,
• and rounded necrotic lesions quickly appear on the liver surface
• disseminated multifocal necrotic hepatitis
Histomoniasis
• Diagnosis
- Epidemiology, clinical signs
- Necropsy
- DD: coccidiosis, tuberculosis, salmonellosis, necrotic enteritis
- Direct observation by microscopy
- Scraping of cecal content, fresh feces
- Histology
- PCR, ELISA
-Treatment • Drugs (most of them are no longer permitted) • Biosecurity (separation of species) • Deworming against Heterakis • Proper litter management
Trichomoniasis
Pathogen
- Trichomonas gallinae (s. hepatica)
- Flagellated protozoa
- 5-9 μm long and 2-9 μm wide
- single-celled, pear-shaped protozoan with 4 whip-like anterior flagella and a fin-like undulating membrane
- Older pigeons carry the pathogen
- The young pigeons show symptoms
- Rarely poult and chicks get sick
Other protozoan infections
• Hexamitiasis • Spironucleus meleagridis • Cochlosoma anatis=>Duct, poult – catarrhal enteritis • Plasmodium (avian malaria) -Transmitted by mosquitos => Erythrocytes, endothel cells • Haemoproteus • Leukocytozoon • Trypanosoma • Toxoplasma • Sarcocystis
Intestinal parasites
- Cestodes, tape worms (flat, segmented, 0.4-40 cm)
- development cycle involves intermediate host
- rarely seen in closed flocks
- decrease in feed intake, egg production, weight loss (in young)
- hemorrhages, necrosis, multiple caseous nodules
- Trematodes (in aquatic environment, <1 cm)
- enteritis, weight loss, mortality with secondary infections
• Nematodes (diagnosis: fecal flotation)
- Upper digestive tract
- Small intestines
- Ceca
- Respiratory tract
Nematodes
-Upper digestive tract: Capillariidae, Tetrameres
• hemorrhages, catarrhal enteritis
• apathy, weight loss, drop in egg production, death (young)
-Small intestines (Ascarididae)
• anemia, intermittent diarrhoea, anorexia, weight loss
-Ceca (Heterakis, Strongyloides, Trichostrongylus)
• Vector for Histomonas meleagridis
-Respiratory tract (Syngamus trachea)
• Small, „Y” shaped, bloodsucking
• irritation, abundant mucus production, hemorrhages, dyspnea
-Treatment: flu-, fenbendazole, levamisole, biosecurity
Ectoparasites
• Permanent (does not live long in the environment)
• scabies
• lice (chewing or biting, Mallophaga) >40 species
• pale yellowish, 1-5 mm, feed on feathers/skin
-chicken body louse (Menacanthus stramineus): often at vent
• direct contact (100s eggs glued to feathers)
• life span 1 month, survive only 1 week after separation
- Signs: pruritus, loss of feathers, excoriations, crusts
- reduced growth rate, decreased egg production, mortality
• Treatment: individual (insecticides), cleaning!
-Intermittent bloodsucking
• mites, ticks, bedbugs, fleas
Intermittent ectoparasites
• Hematophagous mites (both can infect humans)
- Poultry red mite (Dermanyssus gallinae) intermittent
• Often in caged layer flocks, feeds at night for 30-60 mins
• change in behavior, anemia, drop in egg production
• carrier of pathogens (ND, avian pox, Salm, E.coli, Staphylococcus)
• Treatment: insecticides, disinfection
-Northern fowl mite (Ornithonyssus/Liponissus sylviarum)
• Permanent (remains on the host)• Prevalent in winter
• Young birds are more susceptible
• Treatment: spray application to the vent
- Knemidocoptes (>17 species), mange
- Permanent parasites (generation span 2-3 weeks)
- Kn. gallinae, Kn. mutans (scaly leg), Kn. pilae (in parrots)
- head, neck, back, upper leg/featherless part of the leg/beak
- KG: pruritus, feather plucking, scaly, thick, wrinkled skin
- KM: lameness, deformed legs and claws, scales
- Treatment: ivermectin, disinfecting
Pests
Beetles
• make dust, penetrate insulation, vectors (Marek, E.coli, Salm)
• Biosecurity measures and insecticide treatment
Flies
• Passive transportation of many pathogens
• Intermediate hosts for parasites
• Manure: well ventillated, dry, biological control, insecticides
Rodents (rats, mice)
• eat and contaminate poultry feed
• transmit diseases
• destroy electric installations and insulations
• Control: elimination, sanitation, trapping, use rodenticides
