dimorphic systemic mycoses

Dimorphic Systemic Dimorphic Systemic Mycoses: Disease Mycoses: Disease situation in Nepal situation in Nepal

Dimorphic Systemic Dimorphic Systemic Mycoses: Disease Mycoses: Disease situation in Nepal situation in Nepal

Dr Kedar KarkiDr 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 Mycoses

Disease Causative

organisms 

Incidence

Histoplasmosis

Histoplasma capsulatumHistoplasma dubosii

Coccidioidomycosis

Coccidioides immitis 

BlastomycosisBlastomyces

dermatitidis  

Dimorphic Systemic Mycoses

Disease Causative organisms 

Incidence

Paracoccidioidomycosis

Paracoccidioides brasiliensis  

Sporotrichosis

Sporothrix schenkii

Penicilliosis marnefffei

Penicillium marneffei

Tissue morphology of dimorphic pathogens:

Mycosis Tisue morphology

Blastomycosis

Large broad base unipolar budding yeast cells (8-10um).

Coccidioidomycosis

Spherules (10-80um) with endospores (2-5um).

Histoplasmosis

Small narrow base budding yeast cells (1-5um; 5-2um in var. duboisii)

Tissue morphology of dimorphic pathogens:

Mycosis Tisue morphology Paracoccidioidomycosis

Large narrow base, multi-budding yeast cells (20-60um).

Sporotrichosis 

Small narrow base budding 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 Mycoses

DiseaseCausative

organisms     

  Incidence

Candidiasis 

Candida albicans andrelated species.

Common

Cryptococcosis

Cryptococcus neoformans 

Common

Aspergillosis

Aspergillus fumigatus etc.  

common

Opportunistic Systemic Mycoses

DiseaseCausative organisms     

  Incidence

Pseudallescheriasis

Pseudallescheria boydii

Zygomycosis (Mucormycosis)

Rhizopus, Mucor, Rhizomucor,Absidia etc.

Opportunistic Systemic Mycoses

Hyalohyphomycosis  

Penicillium, Paecilomyces, 

Beauveria, Fusarium,

Scopulariopsis etc.

common

Phaeohyphomycosis

Cladosporium, Exophiala, Wangiella,Bipolaris, Exserohilum, Curvularia.

Penicillosis marneffei

Penicillium marneffei common

HyalohyphomycosisDescription:

• A mycotic infection of man or animals caused by a number of hyaline (non-dematiaceous) hyphomycetes where the tissue morphology of the causative organism is mycelial.

Description:

• This separates it from phaeohyphomycosis where the causative agents are brown-pigmented 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 broad-spectrum 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 Background• Bihar Nalanda (1983)• In Nepal Banke(1986) First time• Sunsari ,Bardiya (1995)• Current Epidemiological situation(1998-

2000)• 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

TREATMENT ATTAIMTED

• Pentasulphate,E.M.Biovet(Pakistan)• Tail docking, anti-septic

dressing,anti-biotic therapy,Ivermectin,multi-vitamin,mineral mix.

• Anti-Deg Nala liquor( oral/ parental) ( Nepal)

•23.6% Acetylarsan, liquor arsenic,Degcure(India

Morbidity and Mortality Data of Degnala Disease,

Nepal, 1998 - 2002

Year No. of Outbreaks

No. of Cases

No. of Death

Case Fatality

Treated

1998 18 1158 143 12.3 1015

1999 8 554 15 2.7 539

2000 19 368 1 0.3 367

2001 13 44 0 0.0 44

2002 55 89 7 7.9 82

113 2213 166 2047

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

MOLDY GRAIN POISONING IN MULE-

HORSE

• 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.

TREATMENT ATTAIMPTED.

• 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.

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

suppress itself

stiffness of joints, lameness, rough coat,

loss of long hair, and hoof sloughing and deformities

Hoof deformities are a classic sign pain for the

animal;

Diagnosis of disease:

• Mainly pre-history of animal, whether animal had been fed the type of plant.

• Analysis of feed fodder in area.• Parasitological Examination.• Examination of skin scrapings.• Blood chemical analysis.• Mycological Examination.

Laboratory Findings.• low blood phosphorus.• Mite.• Protein deficient in fodder.• Presence of Blastomyces spp,

Candida spp,Absidia spp., in hoof scraping

TRUE SYSTEMIC (ENDEMIC) MYCOSES• Blastomycosis:• Chronic cutaneous and osseus

disease • lesions on the skin • damage to the vertebrate, ribs,

skull, and bones