Review of Spiking Illness Syndrome of Broiler Chickens in Nepal ;2008

8/14/2019 Review of Spiking Illness Syndrome of Broiler Chickens in Nepal ;2008

http://slidepdf.com/reader/full/review-of-spiking-illness-syndrome-of-broiler-chickens-in-nepal-2008 1/39

Review of Spiking illness

Syndrome in Broiler Chickens:2008:in Nepal

Dr.Kedar Karki



Background:

A sudden and unexpected increased in

mortality in broiler.

Age:8-16 days.

Location :Chitwon, Kathmandu Valley.

Mortality lasted for 3-5 days



Clinical picture:

Affected birds recumbent.

Depressed.

Often went to star-gazing spasm.

Hurdling of the birds.

Trembling.

Blindness.

Loud chirping



Clinical picture:

Litter eating.

Ataxia.

Comatose.

Birds dead with breast down and feet ,legs

straight out behind



Postmortem lesions:

Hemorrhage in liver with necrosis of liver

cells.

Regressed thymus.

Regression of bursa of Fabricius.

Dehydration with accumulation of kidney

Urate.



Postmortem lesions:

Fluid in crop, Fluid in lower gut, watery

contents in ceca

Yellow elastic shanks.

Swollen joints.

Molted appearance. Of brain



Laboratory investigation:

Mycobiota/Microbiota of postmortem tissue

Lung,liver,Proventriculus,Gizzard,Brain,Spleen

Total samples:298

Negative: 24

Mycology; Aspergillus spp, Penicillium spp, in 182

samples, Salmonella spp 24

Mixed E.coli and Staph 68



Treatment provided

Liquid toxin binder like toxolivum

Immunomodulaters,immunocare

Multivitamin B-complex

Liquid microminirals.in water has given

promising result in Kathmandu valley area out

break



Acute aspergillosis

inappetance, depression, polydipsia,

polyuria, dyspnoea, cyanosis

= sometimes, sudden death without any

signs



Chronic aspergillosis

signs are dependent on the area of

invasion

change in voice

respiratory stridor

exercice intolerance

ataxia, torticollis, seizures

conjunctivitis, keratitis beak malformation…



air sacculitis

meningo-

encephalitis

arthritis

uveitis

CLINICAL PICTURES



Postmortem lesions



Common lesions observed in field

cases of Spiking Illness



Affected flock



Review of History

Spiking mortality syndrome of chickens has

been classified as such for approximately ten

years. During the first experiences with the

disease a number of causative agents wereimplicated, yet the symptoms remained

relatively the same.



Review of History

1988 to 1990 the syndrome reached critical epidemic

proportions particularly in the Delmarva area of the

U.S.

Isolated cases were also reported at that time in

Georgia, Alabama and Arkansas.

In 1990 the problem became so severe that a task

force was developed in the Delmarva area in order to

bring some definition to the syndrome.



Review of History

Approximately around 1992, the incidence of

spiking mortality in chickens took a severe

jump in Georgia and to a lesser extent

Alabama. Sporadic cases were also still beingreported in the Delmarva/North Carolina area.



Review of History

Several possible causes were implicated, but nothing conclusivewas identified.

Since that time Dr. James Davis of the Georgia PoultryLaboratory, in conjunction with several researchers across theU.S., conducted exhaustive and extensive research and

uncovered an emerging virus with other interesting revelations.The conclusions of the Delmarva task force and the researchfindings of Dr. Davis have helped to reduce the severity of aflock that experiences SMSC. Yet, the syndrome still occurs andno absolute eradication of the problem is in sight.



Review of Symptoms

The general symptom of spiking mortality in

broilers is a sudden and unexpected jump in

mortality from 8 to 16 days of age. The

mortality lasts for three to five days, after which, the mortality patterns return to a

relatively normal level.



Review of Symptoms

Affected birds become recumbent, depressed

and often go into a star-gazing spasm. Death

often occurs within two to six hours after the

onset of the symptoms. Characteristically,birds that exhibit clinical symptoms but

survive the acute phase, will continue to be

unthrifty and stunted for the rest of the grow-

out.



Review of Symptoms

surviving birds may weigh as little as one half

of the weight of unaffected flock-mates by the

end of the grow-out cycle.



Review of Symptoms

lesions and symptoms into Type A and Type

B.



Review of Type A

Type A was defined as any house of birds experiencing a dailymortality of >5 birds per 1000 between 8 to 16 days of age.

The symptoms must occur for a duration of not more than threedays, with birds exhibiting all or a portion of the physical signsand lesions characteristic of the syndrome. Those signs

included, huddling of the birds, trembling, blindness, loudchirping, litter eating, ataxia, comatose, birds dead with breastdown and feet and legs straight out behind birds. Males arepredominantly affected and survivors exhibit great variation insizes.



Type A

Lesions described with this syndrome include

hemorrhages in the liver with necrosis of liver

cells, regressed thymus, regression of the

bursa of Fabricius, dehydration with theaccumulation of kidney urates, fluid in the

crop, fluid in the lower gut and watery

contents of the ceca.



Type B

Type B spiking was defined as any house of

birds exhibiting a significant mortality during

the ages of 8 to 16 days of age. The mortality

may extend longer than three days but therate is less than five deaths per 1000 per day.

Also the Type B affected birds did not exhibit

the symptoms and lesions of the Type A

affected birds.



"Type"

Regardless of the "Type" of spiking mortality,

one of the hallmark lesions is hypoglycemia

or low blood sugar. Also most cases have

been refractive to supplemental medication or feed changes.



Causative Agents

A number of causative agents have been

implicated in this devastating syndrome.

Mycoses :Aspergillus spp; Penicillium spp

in Nepal Mycotoxins

Feed ingredients

Management

Viruses



Mycotoxins

Mycotoxins or a microtoxin were first

implicated. This was based on the evidence

of liver lesions and trace-back examinations

of affected flocks. Through trace-backinvestigations, several investigators found

that affected farms received feed containing

feed ingredients from specific geographic

locations in the U.S.



Feed ingredients

Feed ingredients have also been

investigated. Investigations by the Delmarva

Task Force studied the possibility of

cocklebur seeds getting into the feed. Nothingwas ever substantiated that cocklebur seeds

were getting into the feed, and laboratory

studies proved inconclusive in reproducing

the syndrome.



Management factors

Management factors were suspected during theearly outbreaks of SMSC by many live productionmanagers. Several ideas were put forth such as coldhalf house brooding, starvation of the birds andstarting chicks on old feed. Substantiation of these

mismanagement situations are difficult to address.However, it is interesting that as some attention hasbeen given to improving management practices, theincidence of SMSC has declined.



Viruses

Viruses were suspected during the initial

outbreaks of SMSC. The Delmarva Task

Force reported on the isolation of an

adenovirus from flocks experiencing thesyndrome. Additional studies on the effect of

an adenovirus have been conducted at the

University of Georgia. These experiments

have also not been conclusive.



An arenavirus

from the feces of chicks exhibiting SMSC. Dr.

Davis' work has shown that higher numbers

of arenavirus particles are found in the feces

of broilers, broiler breeders and commerciallayers experiencing enteritis. However, the

feces of chickens experiencing spiking

mortality, have particularly high numbers of

virus particles.



An arenavirus

Arenaviruses are known to infect mice, other

rodents, birds and men. The virus infects

areas of the brain that regulate hormone

levels in the body, particularly growthhormone. Mice infected with the arenavirus

have been found deficient in growth hormone

which results in hypoglycemia and growth

depression.



Syndrome Solutions

As there have been a number of different causative agentssuggested, there have been a number of suggested treatmentsand preventative measures.

The only successful treatment of SMSC in the face of anoutbreak has been the therapeutic use of quinolone antibiotic in

the water. Other remedies tried have included, changing feed,vitamin supplementation in the water, and adding sugar to thedrinking water. No consistent success have been achieved withthese treatments.



Syndrome Solutions

A number of management techniques have

been employed to reduce the chance of

SMSC. Some common-sense measures such

as adequate warming of the post-broodchambers, rodent control and darkling beetle

control appear to have offered some help.



Syndrome Solutions

One technique that has offered the best help in

reducing the incidence of the syndrome is a lighting

program, which restricts the amount of light the

broilers are exposed to. The theory of the lighting

program is to increase the amount of darkness thebroiler is exposed to as the bird matures. The effect

of this is to increase the level of melatonin (a natural

hormone released from areas of the brain).



Syndrome Solutions

Higher levels of melatonin may help to

elevate the level of growth hormone and

reduce the opportunity for hypoglycemia.

Thus far, it appears that the lighting programhas been successful both experimentally and

in practical usage. However, the lighting

program has not proven to be a cure-all.

Sporadic outbreaks of SMSC still occur regardless of what management practices

have been employed.



Conclusions

Avian aspergillosis »

= not a single entity but a complex of

several diseases…

poor prognosis importance of prophylactic-procedures Réduction of fungal contamination

Chimioprevention ?

Review of Spiking Illness Syndrome of Broiler Chickens in Nepal ;2008

Documents

Transcript of Review of Spiking Illness Syndrome of Broiler Chickens in Nepal ;2008