AVIAN VIRAL AND BACTERIAL RESPIRATORY DISEASES

Presented By

Dr. Ahmed Ragab El-Bestawy

BVs, MVs & Ph.D.

Lecturer of Poultry Diseases

Fac. Vet. Med., Damnhour Univ.

Diseases causing Resp signs:

o Viral: AI, ND, IB,ILT, TRT, Adeno, Reo, Pox wet form and

MD ( non specific)

o Bacterial:

IC, MG, Ecoli, FC, ORT and Chlamydia.

o Fungal: Asperigellosis.

o Parasitic: Syngamus trachea, Cryptosporidium

o Nutritional: Vit A .

o Miscellaneous: Chilling and Ammonia

E.coli

Influenza Virus

Family Orthomyxoviridae

Three main types

Type A

Multiple species

Type B

Humans

Type C

Humans and swine

Influenza A

Multiple species

Humans

Avian Influenza

Most virulent group

Classification by surface antigens

into subtypes

Hemagglutinin (H or HA)

Neuraminidase (N or NA)

Surface Antigens

and Subtypes

18 HA and 11 NA for influenza A

Hemagglutinin (HA)

Function: Sites for attachment to infect host cells

Neuraminidase (NA)

Function: Remove neuraminic acid from mucin and

release from cell

Influenza A

Avian Influenza

Pathogenicity based on genetic features and/or

severity of disease

in poultry

Low pathogenic AI (LPAI)

H1 to H18 subtypes

Highly pathogenic AI (HPAI)

Some H5 or H7 subtypes

LPAI H5 or H7 subtypes can mutate

into HPAI

H9N2 infection

H9 subtype viruses generally exist as low pathogenicity influenza viruses causing mild to moderate disease. However, they have been associated with severe morbidity and mortality in poultry as a result of co-infection with other pathogens.

The first H9N2 influenza virus was isolated from turkeys in Wisconsin in 1966.

H9N2 subtype influenza viruses were isolated from pigs in Hong Kong in 1998 and subsequently from two sick children in 1999; six additional human infections were reported from China

Recent studies have shown that H9N2 viruses may have contributed to the genetic and geographic diversity of H5N1 viruses.

During the last two decades, antigenic and genetic analysis of H9N2 isolates showed their gradual and complex evolution revealing extensive re-assortments to generate multiple novel genotypes (7) with gene segments from different lineages.

Transmission pathways:

Low biosecurity is a high risk.

Market systems

Mainly Air born

Pathogenicity:

Severe morbidity and mortality in poultry results from:

1. co-infection with other pathogens.

2. Live Vaccines (ND &/or IBV)

3. Management factor.

Organ affinity:

Respiratory

Renal

Reproductive

Nervous

Clinical signs and PM lesions

Broilers:

Swelling of head.

Respiratory sound.

Decreased feed in take.

Intestinal ballooning.

Pancreatitis

Nephritis

Layers and Breeders:

Depression and slight to moderate decrease

of egg production.

Intestinal twisting and egg peritonitis

Pancreatitis (Thickening of pancrease)

Nephritis

H5N1 infection

H5N1

: : ( )

1.

2.

3.

4.

5.

6.

7.

. 8.

. 9.

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H9N2 vaccines

Inactivated vaccines

Must be Autogenous

Country/regional variation

Vaccine use will:

Prevent clinical signs

Reduce virus shedding

Dose of the vaccine 0.5 ml .

Administration S/C lower back of the neck .

Age of vaccination:

Broiler one Dose at 7-10 day old .

Breeder & layer 1st Dose 10 D.O

2 nd Dose 40 D.O

3 rd Dose 16-18wk .

Currently available H5 vaccine

A. Inactivated homologous vaccine : B. Inactivated heterologous vaccines: The vaccine have the same H type as the field but

heterologous neuraminidase. Clinical protection and reduction in viral shedding are ensured

by the immune reaction caused by H and N used as marker of field infection.

Dose of the vaccine 0.5 ml .

Administration S/C lower back of the neck .

Age of vaccination:

Broiler one Dose at 7-10 day old .

Breeder & layer 1st Dose 10 D.O

2 nd Dose 40 D.O

3 rd Dose 16-18wk .

Mareks with H5

Fowl Pox with H5

Other vectors as ILT or lasota with H5

Avian Mycoplasmosis

Mycoplasmas are bacteria that lack cell wall and

belong to the class Mollicutes.

.

Species usual host A.Laidlawii Various

M.Anatis Duck

M.Anseris Goose

M.Butenois Buteo Hawk

M.Cloacale Turkey,goose

M.Columbinasale Pigeon

M.Columbinum Pigeon

M.Columborale Pigeon

M.Corogypsi Black Vulture

M.Falconis Saker Falcon

M.Gallinarum Chicken

M.Gallinaceum Chicken

M.Gallisepticum Chicken,turkey,house

finish.

M.Gallopavonis Turkey

M.Glycophilum Chicken

M.Gypis Griffon Vulture

M.Imitis Duck,goose,partridge

M.Iners Chicken

M.Iowae Turkey

Species usual host M.Glycophilum Chicken

M.Gypis Griffon Vulture

M.Imitis Duck,goose,partridge

M.Iners Chicken

M.Lipofaciens Chicken

M.Meleagridis Turkey

M.Pullorum Chicken

M.Sturni European starling

M.Synoviae Chicken,turkey

M.Gallorale Chicken

Major mycoplasma species in poultry

1.M. gallisepticum:

Chronic respiratory disease(CRD in chickens and infectious sinusitis in turkeys)

embryo mortality, lameness, eye lesions.

2. M. Synoviae:

Infectious tenosynovitis in chickens

Respiratory disease(Turkeys), embryo mortality.

3. M. Meleagridis:

Respiratroy disease, leg weakness, embryo mortality in turkeys.

4. M. iowae: embryo mortality, leg abnormalities in turkeys.

MYCOPLASMA GALLISEPTICUM INFECTION

Commonly known as chronic respiratory disease (CRD) of

chickens and infection sinusitis in turkeys.

Characterized by respiratory rales, coughing, nasal

discharge, ,conjunctivitis ,growth retardation and drop in

egg production in layers.

ECONOMIC SIGNIFICANCE

1. Increased condemnations (air saculitis) (5-10%)

2. Increased downgrading of carcasses (10-25%)

3. Reduced feed efficiency(5-15%)

4. Reduced egg production (10-20%)& efficiency

5. Increased embryo mortalities (5-20%)

6. Increased mortality rate (5-30%)

7. Increased medication costs

8. Increased costs of prevention and control ,include

surveillance (serology,culture,isolation, and

identification)

Cause

Mycoplama Gallispticum

. .

.

Transmission- MG/MS

Vertical (transovarian)

MG/MS are transmitted in eggs laid by infected

breeders

Peak transmission is minimal < 3% of eggs

Horizontal Transmission:

Dust, equipments, wild birds as sparrows, trucks, feed, workers, vet. doctors, insects as cats, dogs, contaminated vaccines.

Infected chickens transmit MG/MS

through aerosols (short distances) contaminated feed and water

MS spreads more rapidly than MG

FEED

Skin:

CCRD

Stress

E coli

Stress

Bad ventillation

Cold

(Temp. Variation)

High amonia

Dust

Mycotoxins

Immunosuppression

Poor feed

Overcrowding

Pathogenic Mycoplasma

MG is an intracellular

microorganisms

The latent status, i.e., when the mycoplasma is not

recognized by the host immune system, may be

explained by its intracellular location due to

environmental pressure, as can be exemplified by the

presence of antimicrobials in host tissues for the

treatment of MG, MS or MM infection of birds.

The frequent changes on surface antigens (antigenic

variations due to defective DNA repair system) allow

mycoplasmas to evade the host immune system, and

facilitate their survival when adhered to the host

respiratory tract

Their pathogenic

mechanism for disease include adherence to host target

cells

Destruction of cilia on endothelial

cells

Mycoplasma gallisepticum Invades Chicken

Erythrocytes during Infection

Clinical

signs

INCUBATION PERIOD

Varies from 6-21 days

Varies depend on :

MG strain virulence

Complicating infection

Environmental and other stressors

1.Coughing

2.Sneezing

3.Gasping

4.Rales

5.Ocular and nasal discharge

6.Decrease in feed consumption

7.Pale comb and head

8.Increased mortalities

Broilers

Mycoplasmosis in Breeders

Reduce egg production (MG free hens laid 15 more eggs

per hen housed than unvaccinated MG infected birds over a

45 week laying period)

lower fertility (MG & MS)

lower egg shell quality

Pipped embryo

poor chick quality

smaller chicks

greater cost per chick

PM lesions

Catarrhal inflammation of sinuses,

trachea, and bronchi.

Air-sacculitis:

:

.

. 1

. 2

3 .

4 .

:

Mycoplasma Score 1. No pericarditis and perihepatitis

2 Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiology

and Economics Research Unit, University of Reading

Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiology

and Economics Research Unit, University of Reading

: 3

E.coli

Infectious Synovitis

Eggshell Apex Abnormality

Options to assist in eradication

effort or to reduce losses

Medication

Vaccination

Medication

1. Treat MG respiratory diseases

2. Reduce egg production losses

3. Reduce MG shedding and transmission.

4. Reduce severity of lesions and clinical

signs.

5. Significantly reduce population of MG in

the respiratory tract.

Antimycoplasmal drugs have been used

to :

Treatment

1.

2.

- 3.

- -4.

5.

6.

7.

8.

CCRD .

Antimycoplasmal Drugs

MIC (g/ml) Antimicrobial

0.048 Tilmicosoin

0.006-0.39 Tiamulin

0.04 Doxycycline

0.05 Enrofloxacin

0.06 Ciprofloxacin

0.08 Lincomycin

0.4-4 Tylosin

0.08 Erythromycin

ANTIMYCOPLASMA PLANNING

BROILER

Dose Days

I 1,2,3

II 20,21,22 (With live vaccines

(ND)

Antimycoplasma Planning

Layer-Breeder Dose Days

I 1,2,3

II

For 3 days (20,21,22)

III For 3 days during the 9th week

IV For 3 days during the 17th week

V Feed additive ( premix ) continously

during laying

MG and MS Vaccination

Vaccine types:

MG

F-strain MG

Strain 6/85

TS-11

Bacterin inactivated

MS

MS-H

MG Bacterin- inactivated

Newcastle Disease

Synonyms

Pseudo fowl plaque

Avian distemper

Pests

Avian pneumoencephilitis

Definition

Its usually an acute highly contagious septicemic disease of domestic and wild birds characterized by respiratory symptoms accompanied or followed by nervous manifestation with high losses in susceptible birds.

(Disease common & serious in Egypt)

Strains of the virus vary in virulence (Pathogenecity):

a) Velogenic strains: Texas, Herts, highly virulence used for challenge. Embryo receiving minimal lethal dose die ( 50hrs ).

b) Mesogenic strains: Komarov, used as a vaccine. Moderate in pathogencity for CE (2-3 day) for ODO & 8-10 wks (death rarely).

c) Lentogenic strains: F1, B1, lasota , low virulence used as a vaccine. Pathogenicity for CE die after 100 hrs. For ODO, 8-10 wks old in apparent disease.

d) Apathogenic: Enteric strains

Pathotyping of NDV strains

ND

Avian Paramyxovirus 1 (APMV-1)

Order: Mononegavirales

Family: Paramyxoviridae

Sub-Family: Paramyxovirinae

Genera: Avulavirus

Serogroups: 9 Serogroups (APMV 1 9)

(PPMV-1): Pigeons & Doves - Antigenic variant of NDV

HN

L, NP, P (V)

Newcastle Disease Virus

NP: Nucleoprotein

P: Phosphorilated protein (Overlapping V gene protein)

M: Matrix

F: Fusion with host cell membrane (Smaller spike)

HN: Hemagglutinin / Neuraminidase activities (Largest spike)

L gene: RNA-Directed RNA polimerase (Nucleocapside)

NP P M F0 HN L

Genomic Features

Enveloped pleomorphic RNA virus

100-500 nm size

Single-stranded; Non-segmented

Negative sense (15kb)

Helical nucleocapside symmetry

(Herring-bone like structure)

NDV

Genome

Features

Lentogenic 112RRQRRF117

Velogenic

Although all NDV isolates characterized to date belong to a single serotype, the avian paramyxovirus serotype 1 (APMV-1), significant genetic diversity has been recognized among different NDV isolates. Historically, NDV isolates have been classified into two major groups (class I and II), based on their genome lengths and the nucleotide sequences of their genomes. Class I viruses are distributed worldwide and have been isolated mainly from waterfowl and shorebirds. Class II viruses have been divided into 11 genotypes (I to XI) with genotypes V, VI, VII, and VIII being the predominant genotypes circulating worldwide. Among these, genotype VII viruses are particularly important given that they have been associated with many of the most recent outbreaks in Asia, Africa, and the Middle East

Antigenicity and immunogenicity

Few antigenic variations

Cell mediated immunity (Local immunity: mainly IgA )

Humoral immunity

Antibodies against fusion protein

Antibodies against HN protein : HI Ab

Passive immunity of the chick

Respiratory Form 109

Neurotropic Form 110

Enteric Form 111

Egg Production 114

ND

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Kind of ND vaccines used for immunization of chickens in Egypt:

A. Live lentogenic vaccines: Prepared from naturally weak strains.

1. F. strain vaccine:

It is used in chicks aged 1-10 days.

Via eye dropping , nasal instillation , beak dipping

Local prepared.

Kind of ND vaccines:

2. Hitchiner B1 vaccine: Used for individual vaccination (Eye).

Massive vaccination (D.W) spraying. Used in chicks aged 1-10 days.

3. Lasota vaccine:( Colone, Avinew ) It is more virulent strain than F & B1. It must used as a second vaccination after the first one with either F or B1 . Its used through DW., or spraying.

Kind of ND vaccines:

B. Live mesogenic vaccine:

As Komarov vaccine, local prepared .

Administrated only by intermuscular I/M.

Used for birds aged not less than 4-6 wks.

Must be in good healthy condition and not in production.

Kind of ND vaccines:

C. Inactivated vaccine (Dead vaccine): Egg propagated (velogenic virus) killed with

formaline with adjuvant. Administ.to chickens & turkeys I/M or S/C. Used for vaccination of chickens previously

vaccinated with ND live vaccine. It gives immunity after 14 days and the immunity

persist for 3-4 m in birds vaccinated at early age and for 10-12 m in birds vaccinated at the age of 18-22 wks.

D. Recombonant vaccine : Its live HVT vaccine Carring F gene of NDV, not

interfere with MDA, apply at 1 DO ,long protect.

Infectious Coryza (IC)

Def.

An acute, highly contagious catarrh mainly of growing or mature chickens usually in the cold winter time causing upper respiratory tract disease (nasal sinusitis), growth rate depression and drop of egg production.

Etiology

Avibacterium paragallinarum (Haemophilus paragallinarum).

H. paragallinarum is a gram-negative nonmotile bacterium.

Culture on sheep blood agar is tiny dewdrop, non-hemolytic colonies ,require both X-(hemin) and V-(nicotinamide adenine dinucleotide NAD) factors for growth

A capsule may be demonstrated in virulent strains.

Strain Classification

The Page scheme was initially developed by using a plate or slide agglutination test to recognize the three serovars, A, B, and C . However, the use of hemagglutination-inhibition (HI) technology has been shown to be a much better method for identifying the Page serovar of field isolates.

It is widely accepted that the three Page serovars represent distinct immunovars, since inactivated vaccines based on any one Page serovar provide no protection against the other two Page serovars

Susceptibility

Infectious coryza is an acute respiratory disease of

chickens.

Mature ages are susceptible.

Mode of transmission

The organism may be introduced by the airborne route

Through direct contact Or indirect contact through feed and water contaminated with nasal discharge.

Infectious coryza occur frequently in fall and winter.

Chronic or healthy carrier birds are the main source of infection within 16 weeks after such birds are moved from the brooder house to growing cages near older groups of infected birds.

Introduction of carrier replacement pullets or males for spiking.

Multiple-age groups.

Vaccines:

Trivalent (A,B,C) thiomersal inactivated bacterins are more effective than formalin one.

A number of adjuvants have been shown to be effec-tive for IC bacterins, in particular, aluminum hydroxide gel, mineral oil, and saponin

108 colony-forming units/ml to be effective.

In breeders, at 18 and 22 weeks of age into the leg muscle.

In layers, at 10 and 14 weeks of age.

Significant immunity for about 9 months.

TREATMENT oxytetracycline , Erythromycin and sulphonamides are

commonly used antibiotics.

It should be noted that drug resistance does develop and hence the performance of antimicrobial sensitivity tests is recommended.

Strains of A. paragallinarum resistant to various antibiotics did not carry plasmids.

Relapse often occurs after treatment is discontinued and the carrier state is not eliminated.

Infectious Bronchitis

Clinical Forms of IB:

1.Respiratory Form (Classical)

2.Renal Form

3.Reproductive Form

4.Digestive Form

5.Muscular Form

IBV exists as scores, more than 360 serotypes. Most differ from each other by 20 -50% of S1

amino acids Classical strains: Massachusetts (M41, H). Connecticut (Florida, Clark 333, ArKansas 99), Georgia (SE17), Iowa 97, Iowa 609, New Hampashire and variant strains: Israel strain (Variant II) QX strain Dutch (D207, D3896, D3128, D212) Delawar (JMK, Halte, Gray) Australia T strain ( kidney lesions ). These strain share common antigen by AGPT. Show variable cross reactions with SNT.

Mode of infection and transmission

1. Air-borne disease. Infection occur through respiratory tract and spread readily by direct and indirect contact

(with 48 hr. between infected and susceptible one).

Carriers and vectors :

Recovered birds may shed the virus for 4-9 weeks (49 days) re-infection may lead to persistence of infection and shedding of the virus for long periods.

Incubation period

Naturally 3-10 days, experimentally 18-36 hrs. but natural spread about 36

hrs. it depend on:

Dose. Aerosol , Route of inoculation.

Symptoms and course : The severity of the clinical and pathological picture of the disease

largely depend on :

Virulence and organ-affinity of strain .

Age and immune status of the birds.

General health condition and presence of complicating secondary or inter-current infection, especially Mycploasma, E.coli, Haemophilus, Adenovirus,

etc.

Symptoms and course

In chicks under 6 wks age :

A: Respiratory form

Cause mortality of 5 to 10% up to 50%. With depression, ruffling, loss of

appetite, gasping, rales, coughing, sneezing and wet eyes. Course of disease is usually 3-6 days.

Layers and breeders

Catarrhal trachitis , bronchitis and pneumonia are common. Red

and yellowish caseaus plugs may be found in the lower part of the

trachea and bronchi, Rhinitis and air-sacculitis are sometimes

present.

(Pericarditis, Peri-hepatitis, air-sacculitis in a complicating by

inter-current MG, MS and secondary E.coli infection)

PM Lesions

Respiratory and Kidney forms

Reproductive form

:

) (

:

.

)

Protectotype ) .

(. 14 )

Causes of failure

Eye drop : 98-100% At 10 days PV

DW vaccine: 56% protection 10 day PV

Hand spray at hatchery : 32% (2wks PV), 86% (3 wks PV).

Automatic spray : 93-97% .

ILT

Infectious Laryngotracheitis (ILT) is a viral upper respiratory tract infection of

chicken which produces severe production losses due to mortality of infected

pullets and adult birds and/or decreased weight gain and egg production.

Severe epizootic forms of ILT show a great respiratory distress, gasping,

expectoration of bloody mucus, and high mortality.

Mild forms of infection, sometimes enzootic, are characterized by mucoid

tracheitis, sinusitis, unthriftiness, and low mortality.

History: ILT was reported in the USA in 1925 and its earliest recorded occurrence in the UK was in 1935 . It is now recognized worldwide .

Introduction

ILT virus is a member of the family Herpesviridae in the subfamily Alphaherpesvirinae . The virus is taxonomically identified as Gallid herpesvirus 1 .

Characteristics:

INIB: Intranuclear inclusions in the trachea and on the

chorioallantoic membrane

Types: only one, differentiated by PCR, Variation in virulence

Cultivation: pocks on the CAM and Syncytia in cell cultures

Latency: ILT virus becomes latent like other herpesviruses

Etiology:

ILT virus strains appear to be antigenically homogenous based on serum-neutralization ,immunofluorescence tests and ELISA . Naturally occurring ILT virus strains vary in virulence from highly virulent strains that produce high morbidity and mortality in exposed chickens to strains of low virulence that produce mild to in-apparent infection .

Susceptibility: -Chicken is the primary natural host of ILT and occasionally pheasants and guinea fowl -All ages are susceptible ,the most characteristic signs are observed in adult birds. -In general males are more susceptible than females and the heavier breeds more susceptible than light.

Mode of infection : Natural portals of entry for ILT virus are through the upper respiratory and ocular routes . Ingestion can also be a mode of infection although exposure of nasal epithelium following ingestion is required with this route . Transmission: Horizontal transmission by Direct contact between infected birds with susceptible birds . Indirect contact through contaminated equipments and buildings with aerosol or expectorant of infected birds . Mechanical carriers such as personnel ,wild birds ,vermin ,cats and dogs . Recovered birds and even birds given attenuated live vaccines ,the birds become carriers .

Horizontal spread:

in droplets from infected birds

- spread often slower than other respiratory diseases e.g. IB, ND.

- other agents may exacerbate disease

Latency:

ILT virus or vaccine becomes latent and can be re-excreted intermittently for many weeks

reactivation due to stress, onset of lay, etc.

Incubation period:

6-12 ds. following natural exposure

.

Gross lesions: Lesions may be found in the conjunctiva and throughout the upper respiratory tract of ILTV-infected chickens ,but they are most consistently observed in the larynx and trachea . A) In mild forms of ILT ,gross lesions may consist only of conjunctivitis ,sinusitis and mucoid tracheitis . B) In severe forms of ILT ,mucoid inflammation is observed early in infection with degeneration ,necrosis and hemorrhage occurring in later stages . -In some cases ,severe hemorrhage into the tracheal lumen may result in blood casts or blood may be mixed with mucus and necrotic tissue . -Diphtheritic changes commonly are seen as mucoid casts that extend the entire length of the trachea .

Prevention and control

Modified Live attenuated vaccines

Used in areas of high risk Often where used routinely afraid to stop Application methods: ED, spray or DW Live vaccines can become latent Beware of adding vaccinated or recovered birds to a susceptible flock

Vaccination

Vaccination program : Layers flocks generally are vaccinated twice before the onset of egg production ;vaccines typically are administered by eye drop at approximately 7 wks. of age and again at approximately 15 wks. (by eye drop ,spray or drinking water.)

Live attenuated ILT vaccines provide immunity when applied via intranasal instillation , eye drop, and orally through drinking water. However, application of ILT vaccines by eye drop method appears to be more protective than application by water or spray. Most vaccines when given by eye drop method had lower mean microscopic lesion scores and higher ELISA titers after one vaccination.

Fortunately, ILT is a slowly spreading (long IP) , controllable disease. If a diagnosis of ILT is obtained early in an outbreak, vaccination of unaffected birds may induce adequate protection before they become exposed.

Emergency vaccination

COLIBACILLOSIS IN CHICKENS

The infection results in elevated mortality in flocks, lower egg production in commercial laying and breeder flocks, degraded broiler growth rate, and a marked reduction in carcass quality and elevated condemnation at processing.

Healthy and sick broilers, layers, and breeders showed the incidence of APEC

infection to be 17.7%, 38.6%, and 26.9%, respectively. Resistance to antibiotics was also found to be high

43% of broiler carcasses condemned

at processing had lesions of

colisepticemia

Definition and Synonyms

Colibacillosis refers to any localized or systemic

infection caused entirely or partly by avian

pathogenic Escherichia coli (APEC), including the

following forms:

1. Colisepticemia (hemorrhagic

septicemia) S

2. Coligranuloma (Hjarres disease) S

3. Air sac disease S

(chronic respiratory disease, CRD)

4. Swollen-head syndrome L

5. Venereal colibacillosis (Acute

Vaginitis) L

6. Coliform cellulitis L

(inflammatory or infectious

process, IP)

7. Coliform peritonitis L/S

8. Coliform salpingitis L/S

9. Coliform orchitis L

10. Coliform osteomyelitis S

11. Coliform synovitis S (including

turkey osteomyelitis complex)

12. Coliform panophthalmitis S

13. Coliform omphalitis/yolk sac

infection L

14. Coliform enteritis L

Antigenic Structure and Toxins

Antigens

H-antigens = Flagellar

K-antigens = Capsular

F-antigens = Pilus

O-antigens = Somatic

Antigens

O-antigens

Somatic (lipopolysaccharide or endotoxin released at cell lysis)

often used in serotyping and antigenic identification

H-antigens

Flagellar (proteins not often used in antigenic identification)

K-antigens

Capsular (polysaccharides associated with virulence)

Pilus (involved in attachment

to cells) F-antigens

Serotypes of E. coli

are classified according to the Kauffmann scheme Currently there are approximately

180 O, 60 H, 80 K and 17F antigens

In most serologic typing schemes only the O and H antigens

are determined (e.g., O157:H7).

Antigenic structure

Colibacillosis Disease

Swollen Head Syndrome.

Swollen head syndrome (SHS) is an acute to subacute

cellulitis involving the periorbital and adjacent

subcutaneous tissues of the head.

Usually occurs following upper respiratory viral

infections (e.g., avian metapneumovirus, infectious

bronchitis virus) & Ammonia aggravates the disease

Pericarditis and green

discoloration of the liver

Salpingitis in a young bird caused by E. coli.

Large caseated masses distending the oviduct

(salpingitis).

Goose breeder with acute peritonitis. Yolk in the

peritoneum.

Omphalitis (Salmonella , Pseudomon ,

Streptococus facaeum, Proteous(

SHS (MG, IB, AI, IBD or high amonia

as preliminary infection)

Arthritis

Panophthalmitis (amonia, Aspergillosis)

Treatment

Sensitivity test.

Ampicillin, fluoroquinolones, chloramphenicol,

oxytetracycline, chlortetracycline, neomycin, gentamicin,

ormethiprim-sulfadimethoxine, nalidixic acid,, polymyxin

B, spectinomycin, streptomycin, sulfa drugs, apramycin,

neomycin,.

monensin (anticoccidial) in feed reduced colonization with

E. coli O157:H7.

Vaccination

Types of Vaccines

A variety of vaccines and vaccination methods have

been developed, including passive and active

immunization:

1. Inactivated vaccines

2. live vaccines

a. Recombinant vaccines

b. Subunit vaccines

3. Immunization against specific virulence factors.

Mutant O2 and O78 APEC with deletions of the genes

cya or crp, which are involved in energy production,

were used as a spray vaccine to immunize broiler

chickens.

Similarly, strain O78 mutants with deletions of galE,

purA, and aroA genes were found to be safe and immunogenic, but provided only moderate protection

against homologous challenge with no protection

against heterologous challenge

Def.

Ornithobacterium rhinotracheale infection is a contagious disease of birds mainly turkey and chickens that causes respiratory distress, mortality, and decreased growth.

The severity of clinical signs, duration of the disease, and mortality are extremely variable and are influenced by environmental factors, such as poor management, inadequate ventilation, high stocking density, poor litter conditions, and poor hygiene.

Ornithobacterium rhinotracheale

ORT

Economic importance of ORT in turkey industry

increased mortality

increased condemnation rates,

decreased growth,

decreased egg production,

Transmission

O. rhinotracheale is highly contagious:

Infection by inhalation.

Transmitted horizontally by direct and indirect contact through aerosols or drinking water.

Vertical transmission occurs as ORT was isolated from ovaries, oviduct, hatching eggs, infertile eggs, dead embryos, and dead-in-shell poults and chicks.

Serotypes

18 serotypes (A- R).

Serotype A was the most prevalent serotype

among chicken isolates (94%) and turkey

isolates (57%) but not in USA and South

Africa.

Serotype C is prevalent in chickens and turkey

in South Africa and USA.

Colony Morphology

On blood agar, very small, non-hemolytic

colonies circular, gray to gray-white, sometimes

with a reddish glow, and convex with an entire

edge.

ORT is a gram-negative, non motile, highly

pleomorphic, short, plump rod-shaped, non

sporulating bacterium.

No pili, no fimbriae, no plasmids, or specific

toxic activities have been reported.

Sprayed, live temperature-sensitive mutant of

O. rhinotracheale vaccine.

Treatment

Amoxycillin, ampicillin, Florfenicol.

INFECTIOUS BURSAL DISEASE (IBD)

GUMBORO DISEASE

Definition

An acute, very contagious, viral disease

of young chickens characterized by

destruction of lymphocytes in the Bursa

of Fabricious and, to a lesser extent, in

other organs.

Etiology

Infectious bursal disease virus is a member of the Birnaviridae family,

named for the bi-segmented double stranded RNA nature of the genome of

its members.

The family has 4 genera designated Aquabirnavirus, whose type species is

infectious pancreatic necrosis virus (IPNV) of fish, molluscs, and

crustaceans; Blosnavirus, whose type species is blotch snakehead virus or

BSNV; Avibirnavirus, whose type species is IBDV, which infects birds; and

Entomobirnavirus, whose type species is Drosophila X virus, which infects

insects.

VP4 & 5

Viral proteins

Role Protein

Encapsidation of viral particle

VP1 RNA dependant RNA

polymerase (Small amount in virus

capsids)

Contain antigenic region responsible for Serotype specific

Elicit neutralizing antibodies (responsible mainly for protection)

VP2 Main capsid protein

Morphogenesis of the virus

VP3 Other major structural

protein nit exposed at the surface

Viral protease (maturation of VP2 trimming peptides during virus assumbly)

VP4

Viral relase VP5

IBD virus non-enveloped and resistant to environmental factors

Can persist for months in contaminated houses as once a house is contaminated with IBDV, the disease tends to recur.

Viruses exhibit different degrees of pathogenicity, variants are recognized

Antigenic types Pathotypes

Serotype 1

A: Classical (standard) strains:

Mild

Intermediate

Intermediate plus

Very virulent or hyper virulent (VVIBDV) (Hot strain)

B: Variant: (antigenically different from classical) and mostly low pathogenic causing only immunosuppression without specific lesions

Serotype 1 (Pathogenic)

Serotype 2 (Apathogenic)

IBDV serotypes 1 and 2 share only 30% antigenic relatedness

Strains of IBD follow one of two courses of

disease depending on the age at which

chickens are infected

Subclinical course

Clinical disease

Variant Strains of IBD

-Subclinical Form-

Infection of susceptible chickens less than 2 weeks of age when chickens are exposed to IBDV during the first two weeks post hatch and have sufficient maternal antibody at time of infection to prevent clinical disease but not viral replication in the bursa.

No clinical signs, No peak mortality as evidenced with clinical IBD, but permanent and severe immunosuppression

More economically important form

Majority of field infections are subclinical

Subclinical form- Perminant immunosuppressive

reduced antibody response to vaccination

strong post-vaccine reactions

Increased susceptibility to concurrent or secondary disease as E. coli, Mycoplasma and NE

Inability to clear vaccine virus

Variant

strains Direct bursal

atrophy

Standard Strains of IBD

-Clinical Form-

Infection of susceptible chickens 3-6wks weeks of age:

Sudden onset, rapid increase in mortality

Clinical signs include ruffled feathers, diarrhea, vent pecking, dehydration, trembling, depression, transient immunosuppression

Clinical Signs

1. Anorexia, depression and ruffled feathers.

2. Whitish or watery diarrhoea.

3. The earliest signs is self vent picking and soiled vent feathers.

4. Dehydration and trembling.

5. In terminal stages of the disease, subnormal temperature, severe prostration and finally death.

Morbidity &

Mortality

In susceptible flocks, there is

high morbidity rate usually

approaching 80%.

Mortality may be nil but can be high as 20-30%

and usually begin at 2nd day post infection and peaking and receding in a period of 5-7 days.

Gross Lesions

Changes in cloacal bursa 2nd day post infection ----- bursa has gelatinous yellowish transudate covering serosal surface with prominent longitudinal striations. By 3rd-4th day ----- bursa is double in size and weight (due to edema and hyperemia). By 5th day -------- bursa returns to its normal weight but it continues to atrophy From 8th day forward --------- bursa is approximately 1/3 its original weight.

Mortality rate Slightly higher

Double Slightly lower Normal

2. Dehydration.

3. Haemorrhages in mucosa at junction of proventriculus and gizzard.

4. Haemorrhages in thigh and pectoral muscles.

5. Increase mucous in intestine.

6. Spleen and liver slightly enlarged.

7.Pale kidney ,nephritis and ureter distended with urates.

Vaccination 1. Live IBD vaccines: (1-14 days)

Divided according to virulence of strains:

Mild strains

Intermediate

Intermediate plus

Hot strains

applied in drinking water, eye drop.

2. Oil-adjuvant, killed IBDV vaccines:

Applied by injection S/C or I/M and used to booster or prolong immunity in breeder flocks.

In ovo vaccination

A more recent concept for the vaccination of chickens for IBD and other agents is in ovo vaccination at 18 days of incubation.

In ovo is a labor-saving technique and may provide a way for vaccines to circumvent the effects of maternal antibody and initiate a primary immune response.

The injected material is a live IBD vaccine, either alone or in combination with an anti-IBDV antibody to form immune complexes

Recombinant vaccines

live recombinant virus vectors expressing IBDV immunogens (VP2) as:

Herpes virus of turkey (HVT) Mareks disease virus

Fowlpox virus

Chick embryo lethal orphan (CELO) virus (Adenovirus)

Newcastle disease virus

Baculovirus

Vaxxitek antigen = Faragher 52/70

Old classical strain

Transmune strain = Winterfield 2512 (= IBD Blen)

Very hot strain

Recombinant vaccines

Immune-complex vaccines

Control of outbreak

*Supportive and symptomatic treatment :

1. Diuretics to increase efficiency of kidney and to prevent precipitation of urates .

2. Immunostimulant as vitamin E and levamisole .

3.vitamin K (for hemorrhage).

3.give coarse of antibiotic to prevent 2nd ry bacterial infection (but its contraindicated in case of nephritis).

Other immun-suppressive diseases

CAV

Reo

Mareks Disease

AL

Big liver Disease

H9N2

H9N2

1. Atrophy of bursa of Fabricious and thymus gland

2. Ciliostasis and affect BALT

3. Decreased antibody production

MG

Enteric Bacteria

Salmonellosis

Infections caused by non-motile Salmonella serotypes (Salmonella entrica subspecies entrica serovar pullorum gallinarum)

PD can cause 10-80% mortality during the first 2 weeks.

FT can cause mortality as high as 26% in chicks during the first month of life.

Infections caused by motile Salmonella serotypes are called paratyphoid (PT) salmonellae.

More than 2500 serotypes (of which 30%

are caused by S. enteritidis and S. typhymurium).

Salmonella infections cause:

High mortality rate especially in young chicks

Drop in egg production

Decreased fertility and hatchability

Arthritis

Nephritis (IBD, ANV, Ochratoxins, High protein ration)

Heart nodules (MD, Coligranuloma and Aspergillosis)

Coliflower Oophoritis

Necrotic Enteritis

NE Caused By C. perfringens is an anaerobic, spore-forming, large Gram-positive rod, which is motile by pili.

It is commensally live in the intestinal tract (lower gut & caecum ).

There are five different types of CP {A-E} where A and C is mainly responsible for NE in broilers.

C. Perfringens Infection causes

1. Impaired FCR.

2. Reduced Weight Gain At Slaughter.

3. Reduced The Average Of Farmers Profit With 33% With High And Low Levels Of The Disease.

4. Increased Number Of Carcass And Liver Condemnation At Poultry Processing Plants.

Pre-disposing factors For NE:

Concurrent coccidial infections with scores 2-3

Removal of antibiotics growth promoter

Long anticoccidial withdrawal periods.

Feed and litter contamination with Clostridial spores have been

incriminated as a source of infection.

Diet is believed to be an important:

Change Viscosity and PH (High level of wheat & Barley

increasing SNSPS)

High Protein in ration

High level of animal by products i.e fish meal

Direct damage to intestinal mucosa (coccidia

infection, mycotoxicosis, bacterial over growth).

Immuno-suppressive such as: CAV, IBD, M.D.

litter high in fiber content, feeding programs e.g.

skip a day starvation, overstocking).

Susceptibility:

NE has been reported in many bird species but mostly in broilers 2-6 wks), layer pullets, adult layer, breeders and turkeys.

Subclinical NE

Subclinical NE

NE

Pseudo-membranes covering the entire mucosa of large segments of SI which resemble a coarse yellow coating.

Cholangiohepatitis:

Most common lesion CC by inflammation of bile tree (Intra-hepatic part most frequently).

1. Gross intestinal lesions

2. Present of liver lesions

3. Microscopically exam of gut smears for coccidia.

4. Bacteriological examination: gut content should

contain at least 1 million often 100-1000 million

CP/gm)

Differential diagnosis

Treatment of NE Treatment of NE outbreaks can be

effectively treated by administration of:

Ampicillin , Amoxicillin ,Lincomycin, Bacterin, and Streptomycin.

Metronidazol

Coccidiosis

Species Specific (no cross-immunity exists between species of Eimeria ).

Host specific.

Tissue specific.

Simple, short and direct life cycle.

High reproductive potential of coccidia in poultry intensifies the potential for severe outbreaks of disease in the modern poultry house (New house disease).

It is a self limiting parasite.

Characteristics of coccidian parasite:

Classification:

- Chickens coccidiosis: I Intestinal II- Caecal

I - Intestinal. coccidiosis

A- Anterior E. acervulina

E. praecox

B- Middle E. necatrix E. maxima

C- Posterior E. brunetti

II- Caecal coccidiosis

E. tenella

Clinical signs: The Common Rule Says That: The species We Don't See Cause More Damage and More Loss.

1- diarrhea from (catarrhal to hemorrhagic,...etc.)

2- dehydration.

3- death.

Significantly damaged and therefore lesser absorbing ability of the intestine membrane. All of this leads to the weakening of the animal, a poorer usability of food and poorer conversion, flock disintegration and growth retardation, lesser body weight, poorer production results.

Diarrhea and dehydration are very common and depending on the type of coccidiosis as well as traces of blood in or bloody feces with consequential anaemia, as well as death of infected units where mortality may be expressed in a very significant percentage. Coccidiosis is primarily a disease affecting young animals.

E. acervulina & E. maxima: Poor weight gain, high morbidity, diarrhea, and sometimes mortality. There is often extreme emaciation, ruffling of feathers , anorexia. Killers (E. tenella & E. necatrix): bleeding, high morbidity and mortality, lost weight gain, emaciation, loss of skin pigmentation.

P.M. lesions

Lesions of the intestine can vary from mild enteritis one score (+ve) to

severe necrotic or hemorrhagic type scores (+++ve) and characterized

by :-

1- sever inflam. in specific location according to Eimeria sp.

2- thicken of intestinal wall.

3- whitish yellow plaques (oocysts).

Caecal coccidiosis may produce ballooning of the cecal pouches, which then fill with blood. A later stage involves cecae filled with material of cheesy consistency, streaked with blood (contains non sporulated oocysts) (whitish yellow plaques) or (caecal cords).

Lesions can often be seen from the serosal surface of the small intestine.

The intestinal mucosa may at first be thin and covered with elongate white plaques, arranged transversely.

The intestine may be pale and contain watery fluid.

E. acervulina

E. acervulina

The intestine may be flaccid and filled with fluid, and the lumen often contains yellow or orange mucus. This condition has been described as ballooning.

E. maxima

E. maxima

E. necatrix

older birds such as brooder pullets or layer pullets 914 weeks old. The intestine often is dilated to twice its normal size (ballooning), and the lumen may be filled with blood and fluid.

E. necatrix

Bloody cecal core E. tenella

Control of coccidiosis

I - Correct the managment:

- avoid humidity.

- avoid over crowdness

- provide good ventilation.

- proper temp.

- Eradication of rodents, arthropods (vectors).

- Disinfectant of the visitors, workers & shoes.

- Separate the old from the young. birds

- Control other disease.

- through cleaning & disinfection before each new flocks.

- periodical removal of litters

wet letter should be changed either completely or partially as possible. Wet areas are found

around drinkers, in corners or beside walls and etc.

II- Destruction of oocyst

- good hygiene

- good disinfectant

Ammonia fumigation

or Ammonia solutions

or Sodium hydroxide.

or Calcium oxide

III- Raise the vitality of the birds:

- good balanced rations.

- supplemented especially by vit K & vit A.

- sufficient amount of ration.

IV Feed additive compounds:

- Used as protective coccidiostate:

-Add from the first day of age to the end of the broilers flocks at ration and add from the first day of age to 12-16 weeks of age at ration in layers flocks.

-Use for non diseased birds & not used as treatment. e.g.:

1- Chemicals coccidiostate

Active principle

1- Halofuginon

2- Rubanoed

3- Dicelazoril

2- Inophores coccidiostate

Active principle

1- Monenzin

2- Salinomycin

3- Lasalocid

4- Maduramycin

5- Semduramycin

- Coccidiostate permit descend of some oocysts which lead to partial immunity

There are two main problems with chemotherapeutic approach to controlling coccidiosis, the emergence of drug resistance (which may be developed after repeated uses of the same drug) and residues. This problem is usually met by changing the anticoccidial drugs overcome the drug resistance as following:

Programs for coccidiosis control:

1- Continous use of single drug:

using one particular anticoccidial in the feed from first day till withdrawal period

2- Shuttle programs ( )

Consists of starter medication, using one particular anticoccidial in the feed usually for the first 3 weeks of growth, followed by a change to another anticoccidial in the grower feed for the finishing period.

3- Rotation programs ( ) :

using one particular anticoccidial in the feed for 2 cycles then change to

another.

Used for breeders and floor reared layers:

Natural wild type vaccine:

Coccivac,Immucox.

Attenuated vaccine:

Livacox, or Paracox.

Vaccination

Immunogenicity of different species: Depending on the coccidian species considered, immunity will develop after one single exposure to the parasite or several exposures to the same species as shown in the following table:

Species No. of Exposure to achieve Immunity.

E. maxima 1

E. Praecox 1

E. brunetti 1-2

E. acervulina 2-3

E. mitis 2-3

E. tenella 3-4

E. necatrix 4-5

VI - Vaccination:

- Administration via feed 3-5 days

or spray (Cabin) 1 day old

or eye of nasal drop 1 day old

- Immunity after 3-4 weeks

Precautions after vaccination:

-Never use a medication which affect any stage of Eimmeria sp.

-Never change the litter for one month following vaccination.

Examination for the chicks periodically to be sure from the presence of oocysts & absence of lesion scores.

Mycotoxicosis & their effect on poultry industry

Mycotoxicosis

Mycotoxins are secondary metabolites produced by

fungi that can enter the human and animal diet

through direct or indirect contamination of cereals

and grains.

There are more than 350 type of mycotoxines

Mycotoxin Fungi Produced Commodities

affected

Aflatoxin(B1,B2,G1,G2) Aspergillus flavus

Aspergillus parasiticus Corn, cotton seed,

peanuts, soya

Ochratoxin (A, B, C) Aspergillus ochraceus

Aspergillus nigr Penicillium verrucosum

Wheat, barley, oats, corn, others

Trichothecenes (DON, T-2, DAS, etc)

Fusarium graminearum Fusarium culmorum

Corn, wheat, barley

Zearalenone Fusarium graminearum Corn, wheat, barley,

grass

Fumonisin Fusarium verticillioides Fusarium proliferatum

Corn

Moniliformin Fusarium moniliforme Corn

PR toxin, patulin Penicillium roqueforti Silage, Grass

Species Single oral doseLD50 mg kg -1 bodyweight

Rabbit 0.30

Duckling (11 day old)

0.43

Chicken 6.30

Effect of bird species on toxicity of

aflatoxin B1

Type of bird Age (days) LD50 (mg/Kg Bwt)

Ducklings 3 0.5

Broiler chicks 1 2.14

Broiler chicks 21 3.6

Leghorn Chicks 1 3.3/3.9

Leghorn Chicks 3 3.4

Leghorn Chicks 10 10.67

Turkey poults 1 4.63

Turkey poults 3 5.9

Turkey poults 21 7.84

Japanese qual chicks 3 16.5

Effect of age on toxicity to LD50 of ochratoxin A (after single oral

administration).

Type of bird Age (days) LD50

(mg/Kg Bwt)

Ducklings 3 0.5

Broiler chicks 1 2.14

Broiler chicks 21 3.6

Leghorn Chicks 1 3.3/3.9

Leghorn Chicks 3 3.4

Leghorn Chicks 10 10.67

Turkey poults 1 4.63

Turkey poults 3 5.9

Turkey poults 21 7.84

Japanese qual chicks 3 16.5

Effect of age on toxicity to LD50 of ochratoxin A (after single oral

administration).

Level producing Immunodepression

Regulations

UE - USA Mycotoxins

5 ppb < 20 ppb Aflatoxin

2ppb 0-2 ppb Ochratoxin

100 ppb < 500 ppb Toxin T-2

< 500 ppb Zearalenone

1000 ppb < 5000 ppb Fumonisin

200 ppb < 1000 ppb Vomitoxin(DON)

MYCOTOXIN TOLERANCES

(Synergism)

level , synergism & duration

animal species , breed, sex, age, general health,

immune status

farm management( storage, Temp., & RH / infections )

toxin-,

animal-

environmental-

Factors influencing Mycotoxines

depend on:

related factors

Growth depression .

Increased mortality .

Increased susceptibility to disease .

Decreased serum protein .

Impaired blood coagulation (Decrease vit K absorption) .

Fatty liver .

Weakened bones (Decrease vit D absorption) .

Poor nutrient absorption .

Principle effects of aflatoxin in

broiler

P. M.

1. Pale bone marrow.

2. Regression of the bursa of Fabricius.

3. Mycotoxins can cause damage to mucosae with which they come in contact.

4. Gizzard erosions.

5. Enteritis of variable degree may be seen.

Produced in moderate and colder climates.

It is stored in fatty tissues.

OTA is also known as a potent immunotoxic, teratogenic,

and carcinogenic mycotoxin.

In addition, OTA ingestion induces intestinal injuries,

including inflammation and diarrhea.

It is nephrotoxic.

Immunosuppressive: decrease immunoglobulin production

and causes lymphocytopenia at 4 ppm.

Ochratoxin

Citrinin:

Nephrotoxic.

Na and K increased excretion.

Inbalance in the minerals and salts PPT of uric

acid crystals inside the kidneys.

At the final stage the nervous signs appear,

(convulsions and death).

Trichothecenes: Mytotoxins produced by Fusarium sp.

Includes more than 100 types.

T--2 toxin LD50(4

mg/kg),

HT-2 toxin

Di-acetoxy-scirpenol

Deoxy-nivalenol (DON)

LD50(27 mg/kg)

Neural toxicity

Necrosis, odema,

hemorrhage of intestinal

tract

Prevention And Control Of Mycotoxicosis

1. Quality control of the raw material all the way through feed mill, delivery, storage bins, at the farm, feed through, litter condition in poultry houses.

2. Storage time must be reduced to minimum esp., in starter feed.

3. Feed bin & handling equipment must be kept clean & disinfectant with 10% clorax.

4. Assure that low moisture ingredients are used & not allowed to become damp.

Decontamination for mold & mycotoxins infestation.

-Ammoniation . -Cleaning all visible mold areas. -Heating or roasting of feedstuffs. -Adding toxin binders (HSCAS) to feedstuffs. Using of mold inhibitors (which inhibitor

should be used & at what conc.?

Propionic acid was the only compound exhibiting cidal action.

Ca. propionate had essentially no effect on mold growth .

Sod. Propionate had essentially mild activity towards mold growth.

The failure of these two compounds to exhibit marked anti fungal activity may be attributable to PH of medium since dissociation of these salts is PH dependent

Mode of action of mold inhibitors:

Mycotoxin binders:

An effective binder or sequestering agent is one that prevents or

limits mycotoxin absorption from the gastro-intestinal tract of

the animal.

In addition, they should be free from impurities and odours.

Be aware that not all are equally effective. Many can impair

nutrient utilization and are mainly marketed, based on in-vitro

data only.

Mycotoxin binding is achieved through both:

1- Physical adsorption

Relatively weak bonding through hydrogen bonding

2- Chemical Adsorption (Chemisorption):

It is a stronger interaction which involves ionic or

covalent bonding.

Inorganic binders

Organic adsorbents

Inorganic binders Inorganic mycotoxin binders are silica based polymers. Examples could include:

zeolites

bentonites

bleaching clays from the refining of canola oil hydrated sodium calcium aluminosilicates (HSCAS) diatomaceous earth numerous clays

There are two types of chemical mycotoxin adsorbent/binder:

Extracts of yeast cell wall

Such materials are biodegradable but can, in some cases, also be vectors of mycotoxin contamination.

Benefits of yeast cell wall are low inclusion, high surface area and certainly no toxic contaminants.

The efficacy of glucomannan-containing yeast products as mycotoxin adsorbents in feeds has been investigated globally with several studies with all animals.

Organic Adsorbents Organic mycotoxin adsorbents are carbon based

polymers.

Bio-Transformation

Bio-Agglutination

Bio-Degradation

How dose Bio-mycotoxin work against mycotoxins:

Bio-Transformation: Bio-Transformation is one of four processes involved in toxicokinetics

A substance biotransformed into a more toxic metabolite (bioactivated) is a greater hazard than a substance that is biotransformed into a less toxic or even non-toxic metabolite (detoxified).

Bio-Transformation:

Some specially selected strains of Bacillus subtlus,

Lactobacillus,

S.faecium,

S. cerevisiae

and other technologies that Bio- Transform, (detoxify) mycotoxins.

Bio-Transformation:

The process by which toxic

or

pathogenic

substances stick to long chain

olygosacharide molecules

Bio-Agglutination:

Degradation via enzymatic activity

Bio-degradation:

. 1.

. 2.

.3.

.4.

. 1.

. 2.

. 3.

. 4.

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