Dimorphic Systemic Mycoses

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Dimorphic Systemic Mycoses: Disease situation in Nepal

Dr Kedar Karki

Dimorphic Systemic Mycoses These are fungal infections of the body caused by fungal pathogens which can overcome the physiological and cellular defenses of the normal animal host by changing their morphological form. They are geographically restricted and the primary site of infection is usually pulmonary, following the inhalation of conidia.

Dimorphic Systemic MycosesCausative Disease organisms Histoplasma capsulatum Histoplasmosis Histoplasma dubosii Coccidioidomycosis Coccidioides immitis Blastomyces Blastomycosis dermatitidis Incide nce

Dimorphic Systemic MycosesCausative Disease organisms Paracoccidioides Paracoccidioidomycosis brasiliensis Sporothrix Sporotrichosis schenkii Penicilliosis Penicillium marnefffei marneffei Incide nce

Tissue morphology of dimorphic pathogens:Mycosis Tisue morphology

Large broad base unipolar Blastomycosis budding yeast cells (810um). Spherules (10-80um) with Coccidioidomycosis endospores (2-5um). Small narrow base budding Histoplasmosis yeast cells (1-5um; 5-2um in var. duboisii)

Tissue morphology of dimorphic pathogens:Mycosis Tisue morphology Large narrow base, multiParacoccidioidomycosis cells (20budding yeast 60um). Sporotrichosis narrow base budding Small yeast cells (2-5um).

Opportunistic Systemic Mycoses These are fungal infections of the body which occur almost exclusively in debilitated patients whose normal defence mechanisms are impaired. The organisms involved are cosmopolitan fungi which have a very low inherent virulence.

Opportunistic Systemic Mycoses The increased incidence of these infections and the diversity of fungi causing them, has parallelled the emergence of AIDS, more aggressive cancer and post-transplantation chemotherapy and the use of antibiotics, cytotoxins, immunosuppressives, corticosteroids and other macro disruptive procedures that result in lowered resistance of the host.

Opportunistic Systemic MycosesCausative Disease Incide organisms nce Candida albicansand Candidiasis Common related species. Cryptococcus Cryptococcosis Common neoformans Aspergillus fumigatus Aspergillosis common etc.

Opportunistic Systemic MycosesCausative Disease organisms Pseudallescheria Pseudallescheriasis boydii Zygomycosis Rhizopus, Mucor, ( Rhizomucor, Mucormycosis Absidia etc. ) Incide nce

Opportunistic Systemic MycosesPenicillium, Paecilomyces, Hyalohyphomycosis Beauveria, Fusarium, Scopulariopsis etc. Cladosporium, Exophiala, Wangiella, Phaeohyphomycosis Bipolaris, Exserohilum, Curvularia. Penicillosis Penicillium marneffei common marneffeic o m m o n

Hyalohyphomycosis Description: A mycotic infection of man or animals caused by a number of hyaline (nondematiaceous) hyphomycetes where the tissue morphology of the causative organism is mycelial.

Description: This separates it from phaeohyphomycosis where the causative agents are brownpigmented fungi.

Description: Hyalohyphomycosis is a general term used to group together infections caused by unusual hyaline fungal pathogens that are not agents of otherwise-named infections; such as Aspergillosis.

Description: Etiological agents include species of Penicillium, Paecilomyces, Acremonium, Beauveria, Fusarium and Scopulariopsis.

Clinical manifestations: The clinical manifestations of hyalohyphomycosis are many ranging from harmless saprophytic colonization to acute invasive disease. Ideally, individual disease states involving invasive fungal infection by a hyaline hyphomycete should be designated by specific description of the pathology and the causative fungal genus or species.

Clinical manifestations: Predisposing factors include prolonged neutropenia, especially in leukemia patients or in bone marrow transplant recipients, corticosteroid therapy, cytotoxic chemotherapy and to a lesser extent patients with AIDS. The typical patient is granulocytopenic and receiving broadspectrum antibiotics for unexplained fever.

Laboratory diagnosis: 1. Clinical material: Skin and nail scrapings; urine, sputum and bronchial washings; cerebrospinal fluid, pleural fluid and blood; tissue biopsies from various visceral organs and indwelling catheter tips.

2. Direct Microscopy: (a) Skin and nail scrapings, sputum, washings and aspirates should be examined using 10% KOH and Parker ink or calcofluor white mounts; (b) Exudates and body fluids should be centrifuged and the sediment examined using either 10% KOH and Parker ink or calcofluor white mounts, (c) Tissue sections should be stained using PAS digest, Grocott's methenamine silver (GMS) or Gram stains. Note hyphal elements are often difficult to detect in H&E stained sections.

3. Culture: Clinical specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar.

Culture of Chrysosporium [left] and Fusarium [right] showing typical colony colour for a hyaline hyphomycete ie any colour except brown, olivaceous black or black.

Causative agents:Acremonium sp., Blastomycoses sp: Khari in Buffaloes Fusarium sp.,:Degnala in Buffoloes Paecilomyces sp., Penicillium sp.,: moldy corn poisoning in horse. HPPGE in Poultry. Scopulariopsis sp.

Proventriculitis and gizzard erosion syndrome Causative agents:Penicillium sp.,: HPPGE in Poultry.

Clinical Symptoms The response to the routine treatment is often poor . Condition has been like malabsorption syndrome, Infectious Proventriculitis, Infectious Runting syndrome, pale bird syndrome . Stunting syndrome. Feed Passage,

Post-mortem lesions Anemic appearance, poor growth. Mucous in URT. Distorted shape of proventriculus,gizzard. Swollen large ,small intestine. Liver pale, enlarged with white spate. Enlarged spleen.

Intestines of a young broiler chick suffering from malabsorption syndrome. They are distended with poorly digested feed. A sample of the faeces produced is shown at the bottom of the picture - poorly digested food enclosed in mucus.

MAS STUNTED VS NORMAL BROILER

MAS NORMAL VS PALE SHANK

MAS - HELICOPTER FEATHERS

RSS UNEVENNESS & STUNTING

RSS CLINICAL SIGNS

RSS PASTED VENT

RSS-CHICKS,HUDDLING

RSS CAKED LITTER

MAS ENLARGED PROVENTRICULUS

RSS - GROSS LESIONS

RSS - GROSS LESIONS

RSS - GROSS LESIONS

RSS - GROSS LESIONS

RSS - GROSS LESIONS

DEGNALA DISEASE: What is your identification?

Historical Background Exist in western Pakistan for nearly half century Got name cases first seen in Deg Nala area mostly buffalo (1929-30) No longer confined around Deg Nala India report of cases Punjab Hariyana (1969-1973) Nepal - 1986

Historical BackgroundBihar Nalanda (1983) In Nepal Banke(1986) First time Sunsari ,Bardiya (1995) Current Epidemiological situation(19982000) Morang, Banke, Bardiya, Chitwon, Saptari, Siraha Sun sari, Parsa,( Endemic foci)

CLINICAL FEATURE Associated with Deg Nala. Off Feed, progressing ematiation, drop in milk production Hair loss from twitch of tail Ascending drying of tail sloughing of tissue of tail end Drying curling sloughing of ear tip Loss of hair, swelling reddening of coronet

CLINICAL FEATURE Associated with Deg Nala. Drying and sloughing of skin at coronet region, leaving raw open wound Cracking of skin at lower extremity of all feet Difficulty on movement Grounding Drying and sloughing of skin on muzzle

Clinical Features Associated with Degnala Disease

Pentasulphate,E.M.Biovet(Pakistan) Tail docking, anti-septic dressing,antibiotic therapy,Ivermectin,multivitamin,mineral mix. Anti-Deg Nala liquor( oral/ parental) ( Nepal)

TREATMENT ATTAIMTED

23.6% Acetylarsan, liquor arsenic,Degcure(India

Morbidity and Mortality Data of Degnala Disease, Nepal, 1998 - 2002Year No. of Outbrea ks 1998 18 1999 8 2000 19 2001 13 2002 55 113 No. of Cases 1158 554 368 44 89 2213 No. of Death 143 15 1 0 7 166 Case Trea Fatality ted 12.3 2.7 0.3 0.0 7.9 1015 539 367 44 82 2047

Treated with Anti Degnala Liquor by Dr. Karki in Banke(2056 f/y)

MOLDY GRAIN POISONING IN MULEHORSE Causative agents:Penicillium sp.,:

symptoms TWISTING OF HEAD ON STARGAZING POSITION. EXCESSIVE SWEATING. AIMLESS BITING TO INNATE OBJECTS. DEATH WITHIN 10-15 MINUTES AFTER COLLAPSING ON THE GROUND.

BACKGROUND OF MORTALITY. A Total 31 adult mules died during o63/2/16---o63/76.

LABORATORY FINDINGS. BACTERIOLOGICAL CULTURE OF TISSUE SPCIMEN,SWAB,BLOOD- NO GROWTH OF ANY BACTERIAL ORGANISM. BLOOD PARASITE.NEGATIVE. TOXIC AGROCHEMICAL RESIDUE IN TISSU-NONE. INTESTINAL PARASITES; MIXED STRONGYLUS Spp.

MYCOLOGICAL CULTURE,MYCOTOXIN ANALYSIS PENICILLUM,ASPERGILUS,CANDIDA SPECIES GROWTH IN MEDIA. 6*10-110*10 CFU/GM OF FEED SAMPLE GROWTH OF PENICILLIUM Spp in FEED SAMPLES. NO AFLATOXIN B1B2 DETECTED IN FEED SAMPLE.

ADVISED FOR PROPER DRYING OF GRAIN BEFORE FEEDING. 2% COPPER SULFATE MIXED IN GRAIN BEFORE FEEDING. COMERCIAL TOXIN BINDERS,VARISHTA,TOXICURB @ 1Kg/tone of grain for 15days. Livertonic,Immunomodulater,Vitamin B complex.

TREATMENT ATTAIMPTED.

Current Situation No more Mortality Reported

Khari DiseaseCausative organisms Blastomyces dermatitidis Blastomycosis Candida spp, Absidia spp.,

Symptoms of disease when it occurre Denudation of hair at tail twitch. Rough coat. Lethargic Inappeatance

Symptoms of disease when it occurre Unconscious movement. Fore part leg at scapula region bow shaped shoulder Rest on knee.

Symptoms of disease when it occurre Chalky powder drops from hoof. Rocker shaped foot, which enables to normal movement. Mortality in some cases. After change in season disease suppre