chicks dying , help....coccidiosis???? any thoughts....

[esther5]

ok an update.
sick chick is far from normal but putting on weight. the others had died by now presumably of starvation as they were emaciated.

the good signs...only one wing was drooping tonight.
she is standing more often than previously when she lay down.
she is putting on weight
both eyes were open again tonight and she seemed more alert.

the bad signs....she is un- coordinated with eating and will miss the target(still being crop fed for most of her food)
her head and neck movements are odd. hard to describe a bit like mild cerebral palsy.
her feet are weak and curl up a bit though she will straighten them when she walks..which she can do now.

without the crop feeding she would be dead. i'm still not sure what is causing this but i have given her st johns wort and will look for some fish oil and vitamin e tomorrow. it can't hurt after all. i continue to add garlic and kefir to her chick crumb puree every day...

 

[NYSAHMof3]

Wow. How strange. Well at least you are making a small improvement.

 

[esther5]

i'm wondering if it could be lymphoid leucosis..i read this is transmitted from mum to egg which would explain why so far only the chicks i bought from the same breeder are affected. an article i read and can't find...said that pullets were more likely to spread the disease , after the first moult it was much less likely and even more so after the second moult. the article said pullet eggs should not be used to breed chicks.

so back to my chicken. i am unsure of the diagnosis but if it is the above, will she as a carrier infect my flock or are they likely not to catch it???? i will try and find out more. it is most often spread vertically but i think young chicks are vulnerable horizontally.

anyone know more than me????

 

[esther5]

i found the link http://www.thecuckoopoultrystudofau...leukosis-ndash-avian-the-wasting-disease.html

it seems to fit ....especially the long incubation period since mine have gone down with it one at a time over a 3 month period.

i need to find out more about how it is transmitted to see if it is safe to keep my pullet going even if it was possible to save her which sounds unlikely if it is LL.

 

[casportpony]

From my book, The AAAP Avian Manual

-Kathy

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]II. AVIAN LEUKOSIS/SARCOMA VIRUSES[/FONT][/FONT]
DEFINITION
The avian leukosis (ALV)/sarcoma group are retrovirus-caused, neoplastic diseases of semimature or
mature chickens. The most common, lymphoid leukosis (LL) is characterized by a gradual onset in a flock,
persistent low mortality, and neoplasia of the bursa of Fabricius with metastasis to many other internal organs,
especially the liver, spleen, and kidney. A relatively new strain of ALV, “J”, probably resulting from the
recombination of endogenous and exogenous viruses, primarily causes myeloid leukosis (myelocytomatosis).
OCCURRENCE
Lymphoid leukosis associated mortality is most common in chickens 16 weeks of age or older. The disease
is worldwide in distribution and widespread in the United States. Virtually all flocks are considered to be
exposed to the virus but infection rates within some flocks have decreased due to efforts at eradication by
primary breeder companies. Overall, the incidence of LL is low (1 or 2%), although occasional heavy losses
can occur. A higher incidence of bursal disease virus may be associated with a reduced incidence of LL. With
ALV-J, meat-type chickens appear to be more susceptible than layers.
HISTORICAL INFORMATION
The first report of LL is attributed to Roloff in 1868. However, the disease was not well characterized until
a basis for its separation from MD was established in 1962.​

24

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]AVIAN VIRAL TUMORS[/FONT][/FONT]
ETIOLOGY
Avian leukosis is caused by a family of retroviruses known as avian leukosis viruses (alpha retroviruses),
which have been classified into 10 subgroups—A, B, C, D, E, F, G, H, I and J. In the United States, subgroup
A viruses are most common and are most frequently associated with LL with ALV-J myelocytomatosis next in
frequency. Subgroup B viruses are occasionally isolated, whereas subgroups C and D are rare. Subgroup E
viruses are common and are considered "endogenous" because they are derived from proviral genes
permanently integrated into the host cell DNA; they rarely are associated with neoplasms. Subgroup F, G, H
and I viruses primarily cause leukosis in species other than chickens. The viruses produce a group-specific
antigen that can be detected in albumen of eggs and body tissues or fluids. ALV-J viruses have extensive
antigenic variation within the strain. The avian leukosis viruses can be cultured in chicken embryo fibroblasts
but most produce no cytopathology and are detected by antigen tests. Simple tests for antigen detection are
available and are used in eradication programs in breeders. Antibody tests are also available and are used to
monitor the status of flocks from which the virus has been eradicated.
EPIDEMIOLOGY
Egg transmission is an important mechanism of spread of avian leukosis viruses. The frequency of infected
eggs is usually low but chicks hatched from infected eggs are permanently viremic (immune tolerant), do not
develop antibody, have an increased risk of death from LL, may lay fewer eggs, and will probably shed virus
into their own eggs thus perpetuating the infection. Chickens also can become infected by contact exposure,
particularly with ALV-J, which is efficient at horizontal transmission. In meat type chickens, ALV-J viremia
negative/antibody positive birds can shed virus and post hatch infected birds become tolerant shedders. Some
chickens, particularly those of greater susceptibility due to endogenous virus infection or absence of maternal
antibody, may transmit virus to progeny as a result of contact infection soon after hatch.
CLINICAL SIGNS
Chickens with LL may present with nonspecific or no clinical signs of disease. Many birds with tumors are
unthrifty or emaciated and have pale combs and wattles. Enlargement of the abdomen may result from massive
enlargement of the liver. Some birds with tumors can be detected prior to death by palpation of an enlarged and
lumpy bursa of Fabricius by insertion of a finger into the cloaca. Birds with skeletal myelocytomatosis may
have observable masses on the shanks, head and thorax. Osteopetrosis of the long bones [

Fig. 1; Leukosis;
Cornell U


] or “boot” shanks may occur. Flocks with high infection rates experience depressed egg production.
LESIONS
1. There are no unique external lesions. Lymphomas [

Fig. 2; Leukosis; Cornell U] are seen in many organs in
chickens 16 weeks of age or older, but are especially common in the liver, kidney, ovary, and bursa of
Fabricius [

Fig. 3; Leukosis; Cornell U]. The white-to-gray neoplastic lesions can be diffuse or are
sometimes focal. If the bursa of Fabricius is incised, small nodular lesions can often be detected that would
not otherwise be obvious. Myelocytomatosis [

Fig. 4; Leukosis; UC Davis] is most common with ALV-J;
however, other tumor types such as hemangiomas can also be seen.
2. Microscopically, the neoplastic cells in lymphoid tumors are uniformly lymphoblastic and the cells are
pyroninophilic. Also, they are nearly all positive for surface immunoglobulin M (IgM). The tumors
originate from bursal lymphocytes (B-cells) in which the proviral DNA of the virus integrates during the
process of replication at a site in the host cell genome close to the

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]c-myc [/FONT]gene, a normal host cell gene with
homology to an oncogene present in avian retroviral strain MC29. Activation of this oncogene is believed
to be the primary event in starting the neoplastic process.
DIAGNOSIS
1. Lymphoid Leukosis can usually be diagnosed after careful consideration of the age of the affected
chickens, the course of the disease and the pattern of mortality in the flock, and the location of gross lesions[/FONT]​

25

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]AVIAN VIRAL TUMORS[/FONT][/FONT]
in a moderate number of typically affected chickens. Involvement of the bursa of Fabricius is nearly
always present, although the lesions may not be detected without incision of the organ and examination of
the epithelial surface. In contrast to MD, bursal tumors are intrafollicular, generally causing a more
nodular enlargement. The characteristic tumor cell has B-cell and IgM surface markers. Molecular
methods are available in research laboratories to detect in the DNA of tumor cells the proviral DNA of
ALV located in close proximity to the

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]c-myc [/FONT]gene.
2. Diagnosis is made more difficult because the lesions of LL often appear similar to those of MD, and can
appear identical to those induced experimentally by reticuloendotheliosis virus. Because ALV is very
widespread in chickens, virological and serological methods offer little help in confirming a diagnosis.
3. Diagnosis of ALV-J is achieved by gross and histopathologic examination of tumors and by virus isolation
from cloacal or vaginal swabs or tumors. Although PCR tests have been developed, the virus mutates
frequently requiring the production of new primers.
CONTROL
1. With LL, because egg transmission is so important and the disease is not very contagious, eradication is the
preferred method of control. Most of the eradication efforts have been conducted by the primary breeding
companies. Many breeders of egg-type chickens have reduced markedly the rate of congenital transmission
in their primary breeders and grandparent stocks through a program of testing dams prior to egg production
and removal of those considered likely to transmit virus to progeny. Some breeders have flocks from
which the virus apparently has been eradicated. Commercial progeny from such breeders should have
lower infection rates and thus should experience less tumor mortality and greater egg production.
2. Although LL is not a disease of commercial broilers, ALV-J is a problem and breeders have made
significant progress in their eradication programs. However, due to the efficient horizontal transmission of
ALV-J, control by eradication is more difficult.
3. Genetic resistance to infection with subgroup A viruses is common in meat-type stocks, but quite rare in
egg-type stocks. When present, this resistance offers an alternative approach to control.
4. There is no vaccine that can protect against tumor mortality. Congenitally infected chicks are
immunologically tolerant and cannot be immunized. Vaccines to immunize parent stock where ALV has
been eradicated is being considered as a means to provide maternal immunity to progeny chicks.
TREATMENT[/FONT]​

There is no effective treatment for LL.

 

[esther5]

it might well be i never know. the only thing that doesnt quite fit is my first death was at about 9-10 weeks then regularly up to now ...they are 17 weeks. so onset was a little earlier than average but if i am lucky it will be a disease transmitted fron mother hen to egg because that way, most of my flock might be safer. i do realize it can be transmitted by contasion but it isnt highly contagious.

sigh. i will have to wait and see. meanwhile do i keep my pullet alive or let her go.

there are 4 more birds from that batch of 13 not yet showing signs of illness.

 

[NYSAHMof3]

How is it going?

 

[esther5]

thank you for asking. i have been away for 3 days . we lost the pullet then i think i found the cause. i had ruled out red mite because i checked at dusk and they didn't show most of the symptoms. well the well birds showed none of them. i have started a thread about it but we had a bad infestation. i feel bad that i didn't know. i did look but wasn't looking late enough at night. i now know you need to treat routinely for red mite. not assume you don't have a problem.

 

[LibertyChick]

Who was taking care of the chicks during the 3 days? Did they see the red mites? How did you determine it was red mites? Was it so many hours after dark?

I lost my rooster a couple weeks ago and he had mites. I could see evidence of his bites during the day even. I checked my girls and they don't seem to have any evidence of mites and I treated with food grade diatomaceous earth as a preventative. I think they may have to be treated frequently with the DE. They are more susceptible if they are sick and nutritionally deficient.

LibertyChick

 

[esther5]

i saw them an hour after it was properly dark in their millions....
dd looked after them while i was away. there have been less every day.

i advise you put vaseline on the ends of the roosting poles. that will let you know if there is a problem as some of them will stick in it.

i saw no evidence on my girls during the day at all.