Not an Emergency...Marek's in the Flock

[casportpony]

I've got one right now that is very sick and probably won't make it... Could be Marek's but won't know for sure until she dies and I send her off for necropsy. If it is Marek's, it's the wasting away form with possible ocular involvement. I don't think I've ever seen a chicken so thin, there's nothing to her! Of course I'll tube feed her and I'll probably start her on some Baytril, but it probably won't matter.

-Kathy

 

[pysankigirl]

I'm so new to chickens I don't even know what MG or MS is. But if its anything like MD I would be hesitant to continue. As I am right now. I sure hope you find out exactly what your flock has.

Thanks. MG is Mycoplasma Gallisepticum and it is a respiratory thing. They get a cough and respiratory rales and eye swelling/messiness that comes and goes throughout their life (from what I understand) The only two that I had that definitely had it I had killed and necropsied by the state. They were still in my quarantine pen, so there is a small chance that my flock doesn't actually have it. There have been no respiratory symptoms in the rest of my flock...just a very occasional sneeze (like once a week.) The mortality rate is quite low but it does lower the resistance to other diseases.

The only sick chicken I currently have is the one girl that has Mareks-like symptoms but I sent her blood off and she doesn't have Mareks.

 

[hogster160]

I've got one right now that is very sick and probably won't make it... Could be Marek's but won't know for sure until she dies and I send her off for necropsy. If it is Marek's, it's the wasting away form with possible ocular involvement. I don't think I've ever seen a chicken so thin, there's nothing to her! Of course I'll tube feed her and I'll probably start her on some Baytril, but it probably won't matter.

-Kathy

Well for her sake, I hope she goes peacefully in her sleep. I know that not easy for us to see, but I've read stories of birds having a spasm freak out thing. I'd much rather peaceful. How long have you been dealing with MD?

Deb

 

[hogster160]

Thanks. MG is Mycoplasma Gallisepticum and it is a respiratory thing. They get a cough and respiratory rales and eye swelling/messiness that comes and goes throughout their life (from what I understand) The only two that I had that definitely had it I had killed and necropsied by the state. They were still in my quarantine pen, so there is a small chance that my flock doesn't actually have it. There have been no respiratory symptoms in the rest of my flock...just a very occasional sneeze (like once a week.) The mortality rate is quite low but it does lower the resistance to other diseases.

The only sick chicken I currently have is the one girl that has Mareks-like symptoms but I sent her blood off and she doesn't have Mareks.

Are there other tests she can have to decide what she has? What does your vet say? or the guys who did the MD testing? Did they have any ideas for you to follow up on?

 

[hogster160]

I have a call into Purdue University, just waiting for them to return my call now. Hopefully I will hear something today.

 

[pysankigirl]

Are there other tests she can have to decide what she has? What does your vet say? or the guys who did the MD testing? Did they have any ideas for you to follow up on?

I wish I had a Chicken Vet in my area. The vet at the testing lab wants me to bring her in for a necropsy. I am going to do the blood test for MG and MS on my entire flock. MS is my next suspect, honestly. It causes "Lameness" (I wish they would be more specific as to what THAT means) It also could be a malabsorbtion problem where for some reason this one chicken isn't absorbing B vitamins correctly.

whatever it is, She is a friggin sweetheart. not sure why this sort of thing always happens to your favorite chicken. so I am trying not to sacrafice her to necropsy if I can help it.

The ironic thing is: the cheapest way for me to get the testing may be to go through the NPIP program so I might become NPIP certified by the end of this...LOL

 

[Haunted55]

The ones that have obvious ocular changes seem like they can still see, they find food, water and their roosts just fine and none have lost any weight.

-Kathy

The occular here seems to be a secondary thing that some get after they recover from the leg involvement. It usually hits around the 6-8 month mark. I've even had a couple that just went blind with no pupil or eye color change at all. It's awful, but all of my survivors are skinny. they were damaged by the coccidiosis and enteritis they got before the symptoms of Marek's were even seen. They're healthy and their feathers, what they have of them are shiny and bright. This is the thing about Marek's that gets me. You have one thing, I can have another and Seminole and Nambroth something entirely different. Kinda the same but just enough different to lead to the question of why.

 

[casportpony]

From the AAAP Avian Disease Manual​

93
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
PREFACE
Mycoplasmas belong to the Order

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasmatales[/FONT][/FONT], are the smallest prokaryotic organism (DNA content)
cultivatable on artificial medium and are completely devoid of a cell wall. The absence of a cell wall accounts
for their pleomorphic shape, fried-egg colony appearance and their resistance to penicillin-like antibiotics. Over
twenty five species have been identified from avian hosts although several isolates are unidentifiable. Generally,
mycoplasmas have a narrow host range. Four mycoplasma species are considered pathogenic to commercial
poultry;

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma gallisepticum, M. synoviae, M. meleagridis [/FONT][/FONT]and [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M[/FONT][/FONT]. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]iowae[/FONT][/FONT]. Pathogenic species generally
infect the respiratory system but other systems maybe involved. Transmission is generally by direct contact
although egg transmission, carrier birds and fomites are of importance. The cultivation of

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma sp[/FONT][/FONT]. is
somewhat demanding and requires specialized media containing 10 – 15% serum, yeast-derived components
and unique factors for certain species. Colony morphology is variable but is characterized by a “fried-egg”
appearance. In general, colony morphology, cultural characteristics or carbohydrate fermentation are not useful
for speciation. Identification to the species level is usually based on immunologic tests utilizing species-specific
antisera or amplified DNA type tests. Inoculation of 5-7 day-old embryos is an alternative isolation procedure
utilized when artificial media is unrewarding. Alternatively, clinical material can be inoculated into young
chickens or turkeys and a comparison of pre-inoculated sera with 3-5 week post-inoculated sera by the
immunologic tests may provide clues as to which

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma sp. [/FONT][/FONT]is involved.
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]I. MYCOPLASMA GALLISEPTICUM INFECTION[/FONT][/FONT]
(MG; Chronic Respiratory Disease; CRD;
Infectious Sinusitis of Turkeys)
(See Table on Page 101)
DEFINITION
A mycoplasma infection characterized by respiratory signs and lesions, a prolonged course in the flock and
primarily affecting chickens and turkeys. In turkeys the disease is frequently manifested by swelling of the
infraorbital sinus (es) and called infectious sinusitis.
OCCURRENCE
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma gallisepticum [/FONT][/FONT]


(MG) occurs primarily in chickens and turkeys but also has been reported in
partridge, pheasants, peafowl, quail, guinea fowl, ducks, and pigeons. All ages of chickens and turkeys can
have the disease although the very young are seldom submitted with MG. Since 1994, a serious

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M.
gallisepticum [/FONT][/FONT]


infection of free-ranging house finches has been shown to cause periorbital swelling,
conjunctivitis and mortality.
HISTORICAL INFORMATION
In the United States the disease was first described in turkeys in 1905, then in chickens in 1935. MG
became of major importance as the poultry industry expanded over the last 25 years. The first of a series of
national conferences on mycoplasmosis in poultry was held in 1962 and recognized the importance of MG.
Considerable progress has been made in the control and eradication of MG, especially in turkeys, but the
disease is still of major importance.
MG is one of the more costly poultry diseases, sharing that distinction in the United States with Marek's​

disease and Newcastle disease. A few years ago the annual loss from MG was estimated at 125 million dollars.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
94
ETIOLOGY
1.

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. gallisepticum is the etiologic agent. However, this organism is often associated with one or more of the
following agents and pathogenicity is enhanced by these associations: infectious bronchitis virus,
Newcastle disease virus, [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Escherichia coli, [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Pasteurella multocida[/FONT][/FONT], and [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Hemophilus paragallinarum[/FONT][/FONT].
2. [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. gallisepticum seldom survives for more than a few days outside of the host. Carrier birds are essential
for its survival.
3. In chickens the organism may be present and cause no disease until triggered by stress, such as changes in
housing, management, nutrition, or weather; vaccination against or infection with infectious bronchitis or
Newcastle disease; or increased levels of dust or ammonia in the environment.
4. [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. gallisepticum strain variability exists and accounts for the variability of host susceptibility, clinical
presentation and immunologic response.
EPIDEMIOLOGY
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M[/FONT][/FONT][/FONT][/FONT]


. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum is transmitted in some of the eggs (transovarian transmission) laid by inapparent carriers.
Infected progeny then transmit the agent laterally, probably through infectious aerosols coughed into the air and
through contamination of feed, water, and the environment. The agent probably can be transmitted by other
species of birds, domestic or wild. In addition the agent can be transmitted mechanically on shoes, feed sacks,
crates, etc.
CLINICAL SIGNS
Signs usually develop slowly in the flock. They vary in severity, depending on strain of organism, and may
persist for weeks or months. Signs are the same as those observed with many other avian respiratory diseases.
They include coughing, sneezing, snicks, rales, ocular and nasal discharge, and, in turkeys, swelling of the
infraorbital sinus (es) in occasional birds. Additional signs are listed below.
1. Adult layers- Drop in feed consumption and egg production. Egg production continues at a lower level.
Mortality is low but there may be many unthrifty birds.
2. Broilers (3-8 weeks old) - Signs are more pronounced than in adult birds and the disease is more severe.
Feed intake and growth rate are reduced. Mortality is variable but may be high, particularly if poor
husbandry, exposure, or other stress factors are present.
3. Turkeys- In addition to swelling of one or both infraorbital sinuses [[/FONT][/FONT]

Fig. 1; M. gallisepticum; AAAP],
infected turkeys may have nasal exudate wiped on their wings. Alternatively, if the air sacs and lungs are
primarily involved, mortality from pneumonia and airsacculitis may be very high although few birds have
swollen sinuses.
LESIONS
1. Poor physical condition and loss of weight are usually apparent and suggest the presence of a chronic
disease.
2. There is marked catarrhal inflammation of the nasal passages, sinuses, trachea, and bronchi. Air sacs often
are thickened [

Fig. 2; M. gallisepticum; AAAP], and opaque and may contain hyperplastic lymphoid
follicles in their wall. Recent vaccination against Newcastle disease or infectious bronchitis may enhance
opacity of air sacs. Air sacs often contain mucoid or caseous exudate.
3. The following classic triad of lesions is often the basis of extensive condemnation of infected birds at
slaughter: airsacculitis, fibrinous perihepatitis, and adhesive pericarditis [

Fig. 3; M. gallisepticum; AAAP].​

These lesions are not pathognomonic and may occur with chlamydiosis or septicemia.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
95
4. In infectious sinusitis of turkeys, lesions may be restricted to swelling of the infraorbital sinuses.
Conversely, sinusitis may be absent although rhinitis, tracheitis, and airsacculitis occur and there may be a
fibrinous pneumonia. Occasional turkeys and chickens may have the oviduct distended with exudate
(salpingitis).
DIAGNOSIS
1. A history of chronic respiratory disease accompanied by lowered feed consumption, poor gains, or lowered
egg production is suggestive of MG. Typical gross lesions are very suggestive.
2. Positive plate or tube agglutination tests for MG on sera from a few birds in the flock strengthen the
diagnosis. Because sera from birds with

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma synoviae may cross-react, it is a good plan to confirm
some of the agglutination tests with the hemagglutination inhibition (HI) test or MG ELISA test. Crossreactions
usually do not occur when the HI or ELISA test is used. Flocks recently vaccinated with oilbased
vaccines may also produce false-positive agglutination tests.
3. A commercial PCR test specific for [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum [/FONT][/FONT]is available. Tracheal swabs from a number of birds
can be tested.
4. Isolation and identification of [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum [/FONT][/FONT]can be cultured from exudate, trachea, sinuses, air sacs, or
lungs on artificial media or in chick embryos. MG identified isolates can be compared by molecular
techniques for epidemiologic purposes.
5. In many instances it will be necessary to differentiate MG from other respiratory diseases of poultry,
usually by culture or serologic tests. Pulmonary and air sac lesions may be confused with colibacillosis and
aspergillosis. In turkeys, fowl cholera is a frequent and important complication and may be accompanied
by a fibrinous pneumonia. Sinusitis in turkeys can also be caused by avian influenza, [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae[/FONT][/FONT][/FONT][/FONT]
infection, and cryptosporidiosis.
CONTROL
1. Depopulation of infected premises should precede establishment of a "clean" flock. Thoroughly clean and
disinfect the houses and leave them vacant for a few weeks.
2. Prevention is based largely on obtaining chicks or poults hatched from eggs from MG-free breeder flocks.
The MG-free progeny are then raised in quarantine. MG-free breeder flocks have been established for both
chickens and turkeys. They are monitored by serologic testing to assure that they and their eggs are free of
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M[/FONT][/FONT]


. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum. Quarantine measures must be strictly enforced and good management and sanitation
must be practiced to keep a flock free of infection.
3. The vaccination of replacement pullets scheduled to enter MG positive layer complexes is practiced in most
states. Three live commercial vaccines (F-strain, TS 11 and 6/85) are available and are administered via
fine spray or eye-drop to birds during the growing period to protect them from clinical disease during the
laying period. The live F-strain MG vaccine is pathogenic in turkeys. An oil-emulsion- based bacterin is
also available for use in replacement pullets destined for multiage egg production complexes where MG is
established in older hens.
4. Many MG-free breeder flocks were established initially by identifying small flocks that were not infected
and using that flock as a nucleus. In addition egg dipping (in antibiotic solutions), heat sterilization, and
antibiotic treatment of hatching eggs have all been used in attempts to obtain disease-free progeny from
infected breeder flocks. All of the latter three methods reduce the number of infected progeny that hatch
from eggs from infected flocks. No antibiotic or drug given to infected breeders will prevent them from[/FONT][/FONT]​

laying some infected eggs.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
96
TREATMENT
1. Marketing an infected flock with a low incidence of the disease may be more economical than treatment
because treatment is very expensive. Consider this possibility initially.
2. Improve the management, husbandry, or nutrition if possible. In particular, try to reduce the dust to which
the birds are exposed if dust is excessive. Remove accumulated manure and improve ventilation if
ammonia levels are excessive. Eliminate all possible sources of stress.
3. Many broad-spectrum antibiotics have been used for treatment and will suppress losses. However, relapses
often occur when treatment is discontinued. Most antibiotics are given in feed or water, preferably in
water. Tylosin and tetracyclines have been used extensively for treatment. Injectable antibiotics may be
more effective if the disease is advanced and if the flock is small enough to be treated individually. Treated
birds must be held off the market for a time to meet regulations designed to prevent residues in meat.
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]II. MYCOPLASMA MELEAGRIDIS INFECTION[/FONT][/FONT]
(MM Infection)
(See Table on Page 105)
DEFINITION
An egg-transmitted mycoplasmosis of turkeys characterized by inapparent venereal infection in breeder
turkeys, airsacculitis in recently hatched poults and late embryo mortality.
OCCURRENCE
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma meleagridis [/FONT][/FONT]


(MM) infection is confined to turkeys and occurs in all age groups. The disease
is usually inapparent except in nonhatching turkey embryos or recently hatched poults in which it causes
airsacculitis. Most large turkey breeder flocks are now free of MM infection.
HISTORICAL INFORMATION
1. Airsacculitis in newly hatched poults was first noted in 1958 but was not considered a major cause of loss
because the lesions usually regressed. Airsacculitis at time of slaughter was usually attributed to infection
with

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma gallisepticum (MG) or [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma synoviae [/FONT][/FONT](MS).
2. After MG and MS infections were brought under control, airsacculitis still remained as a significant cause
of condemnation at slaughter. MM infection was found to be the cause.
3. [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. meleagridis has been eliminated from the major primary turkey breeders. Infection in commercial flocks
is not uncommon.
4. Skeletal abnormalities have been referred to as TS-65 (Turkey Syndrome 65) and crooked necks
abnormalities have been referred to as wryneck.
ETIOLOGY
1. The etiologic agent is [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]meleagridis[/FONT][/FONT]. The organism is fastidious in its growth requirements and,
presumably, easily destroyed by environmental factors and most disinfectants.[/FONT][/FONT]​

2. Concurrent infection with other mycoplasmas can occur and increases the severity of lesions.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
97
EPIDEMIOLOGY
1. Infected breeder hens lay some eggs containing

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]meleagridis[/FONT][/FONT], transmitting mycoplasma to some of their
progeny. Organisms are spread laterally to many hatchmates via aerosols from the respiratory tract or to
the vent on contaminated hands during vent-sexing.
2. In some progeny, the organism later spreads to and localizes in the reproductive tract. In male turkeys
localization is often in the cloaca and/or phallus and their semen may contain the agent.
3. Artificial insemination of turkey hens with pooled infected semen is an important method of MM spread.
4. Most tom and hen turkeys overcome MM infection after one breeding season. By then the infection has
already been transmitted to many of their progeny.
5. MM has a distinct predilection for the bursa of Fabricius and can cause immunosuppression, which may
explain why infected turkeys are more susceptible to other infections, especially colibacillosis.
CLINICAL SIGNS
Most of the following signs are mild or inapparent on casual examination and go unobserved.
1. Often there is impaired hatchability of eggs from infected flocks. Embryo mortality is highest after eggs
are transferred to the hatcher and at pipping.
2. Poults hatched from infected lots of eggs may have a high incidence of starveouts and may make poor
weight gains.
3. Young growing poults may show mild respiratory signs and occasional poults may have sinusitis.
4. Small numbers of poults may have skeletal abnormalities associated with a deforming osteomyelitis in
cervical vertebrae (crooked neck) or leg deformities.
5. Adult breeders usually show no signs [[/FONT][/FONT]

Fig. 1; M. meleagridis; AAAP] of venereal or respiratory infection.
LESIONS
1. Infected, pipped, unhatched embryos and recently hatched poults have a variable degree of airsacculitis
[

Fig. 2; M. meleagridis; AAAP] manifested by thickening of air sac membranes and possibly by the
presence of small amounts of yellow exudate in the air sacs [

Fig. 3; M. meleagridis; NCSU]. In
uncomplicated MM, lesions regress and disappear in most turkeys by marketing time.
2. Poults with wryneck may have a cervical airsacculitis and osteomyelitis of adjacent vertebrae that can be
demonstrated microscopically.
3. Adult breeders are free of gross lesions of the genitalia. However, outbreaks of airsacculitis, synovitis, and
sinusitis have been observed in mature and semimature turkeys from which only MM could be isolated.
4. MM can also cause a generalized skeletal disorder historically known as turkey syndrome 65 (TS 65)
characterized by chondrodystrophy, or unilateral or bilateral varus deformities [

Fig. 4; M. meleagridis;
AAAP


] and perosis.
DIAGNOSIS​

1. Monitor pipped embryos and weak, cull poults for the presence of air sac lesions.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
98
2. Diagnosis can be made by the isolation and identification of MM from infected tissues or exudates. The
organism is fastidious and requires special media. Isolates must be differentiated from MG, MS, and other
mycoplasmas by serologic methods or fluorescent antibody techniques.
3. Turkeys infected with MM develop antibodies in 3-5 weeks. These antibodies can be demonstrated by
plate and tube agglutination tests. Positive reactors can be confirmed by hemagglutination inhibition tests.
These tests alone are not adequate for eradication of infection but can indicate infection in a flock. Test
antigens are commercially available.
CONTROL
1. Poults should be obtained from MM-free breeder flocks.
2. A breeder flock free of MM infection can be established by inoculating all of the turkey eggs for hatching
with 0.6 mg of gentamicin sulfate and 2.4 mg of tylosin in a 0.2-ml volume. Injections are made into the
albumen through a small hole made by a dental drill in the small end of the egg. The newly hatched flock
is monitored by culturing pipped (unhatched) eggs and 1-day-old cull poults and by using the plate
agglutination test on sera from the flock.
3. Dipping the eggs from infected breeder flocks into solutions of tylosin or gentamicin will substantially
reduce the incidence of infection in the progeny. Dipping is often combined with temperature- or pressuredifferential
techniques.
4. Repeated serologic testing alone has not been successful in establishing clean flocks. However, both egg
dipping and testing programs have value.
5. Poults are often injected with an antibiotic during servicing in the hatchery, which probably aids in
reducing MM infections.
6. Treatment of semen with antibiotics results in an unacceptable decrease in sperm viability.
TREATMENT
Because MM is sensitive to tylosin and tetracyclines, they may be of value in controlling airsacculitis in
infected turkeys. It is unlikely they would be effective in controlling venereal infection. Use of
lincomycin/spectinomycin in the drinking water (2 g/gal) for the first 5-10 days of life reduced the incidence of
airsacculitis and improved weight gains.
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]III. MYCOPLASMA SYNOVIAE INFECTION[/FONT][/FONT]
(MS, Infectious Synovitis; Tenovaginitis)
(See Table on Page 105)
DEFINITION
Predominately a subclinical upper respiratory infection of chickens and turkeys. Systemic infection results
in an acute or chronic condition of chickens and turkeys characterized by inflammation of synovial membranes
and, usually, by exudate in the joints and tendon sheaths of many infected birds. Synovial involvement is
referred to as infectious synovitis.
OCCURRENCE
Respiratory

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. synoviae infections are common in multi-age commercial layer flocks and are
predominately subclinical. The Infectious Synovitis form occurs in chickens, especially in broilers, but the[/FONT][/FONT]​

disease also occurs in turkeys. The disease is usually seen in young (4-12-week-old) chickens or young (10-12-

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
99
week-old) turkeys. It has been seen in adult layers and in chicks as young as 6 days of age. Synovitis occurs
throughout the year but is more severe during the cold, damp seasons or whenever the litter is wet. The disease
is probably worldwide in distribution. The incidence of the disease has greatly decreased in recent years in the
United States.
HISTORICAL INFORMATION
Infectious synovitis was first described in chickens in 1954 and in turkeys in 1955. Although the disease
was uncommon initially, it is now well established. It is said to be less commonly encountered today than a
decade ago.
ETIOLOGY
1. The etiologic agent is

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae (MS), a fastidious organism that requires nicotinamide adenine
dinucleotide for growth. There appears to be only one serotype of the organism, although isolates vary in
pathogenicity.
2. [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae is a fastidious organism. It can usually be grown in 5-7-day-old embryonating chicken eggs or
in special mycoplasma media. A commercially available PCR test can rapidly identify a MS positive flock.
3. Convalescent sera from birds with [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. synoviae will agglutinate commercially available [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae plate
antigen. During the early stages of synovitis the sera may also agglutinate [/FONT][/FONT][/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma gallisepticum plate
antigen. Cross-reactions usually do not occur when hemagglutination inhibition (HI) or ELISA tests are
used to separate [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. synoviae from [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum infection.
EPIDEMIOLOGY
1. Transovarian transmission is an important means of spread of the infectious agent. Only a small number of
eggs from reactor birds carry [/FONT][/FONT][/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae and most of them are laid during the earlier stages of infection.
2. Infection also spreads laterally via the respiratory tract. Such spread is slow and only part of the infected
birds develop joint lesions.
3. The organism has a predilection to localize in synovial-lined structures such as joints, tendon sheaths and
bursas (breast blisters). It also localizes in the ovary and, occasionally, in the air sacs or sinuses.
CLINICAL SIGNS
1. Lameness in many birds and a tendency of affected birds to rest on the floor are prominent early signs.
Many affected birds have pale head parts and swollen hocks or foot pads. The feces of acutely affected
birds often are green. Eventually, affected birds become dehydrated and thin because of failure to eat and
drink regularly.
2. Morbidity is usually low to moderate but may be high if there is damp, cold weather or the litter is wet.
Mortality is usually less than 10% unless there are other diseases present or the husbandry is poor.
3. A slight, transient egg production drop maybe observed in acutely infected layer flocks.
4. Respiratory tract infections are usually asymptomatic.
LESIONS
1. In the early phase of synovitis most synovial-lined structures (joints, tendon sheaths) contain a sticky,
viscid, gray to yellow exudates [[/FONT][/FONT][/FONT][/FONT]

Fig. 1; M. Synoviae; AAAP]. This is usually more voluminous in swollen​

hock or wing joints or under swollen foot pads [

Fig. 2; M. Synoviae; AAAP].

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
100
2. In later stages of the disease the birds may be emaciated or thin and there may be no lesions in internal
organs. Exudate in joints and tendon sheaths may be inspissated or joint surfaces may be stained orange or
yellow. Breast blisters often are present secondary to trauma from resting on the floor.
3. Respiratory lesions may be absent or consist of a mild mucoid tracheitis, airsacculitis, or sinusitis, lesions
that are usually associated with

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum infection (chronic respiratory disease). Such birds may
not have the usual lesions of synovitis described above.
DIAGNOSIS
1. Typical signs and gross lesions, especially epizootic lameness and characteristic exudate in swollen joints
or tendon sheaths, are suggestive of synovitis. The diagnosis can be strengthened by obtaining positive
plate agglutination tests for synovitis on sera from a few birds in the flock. Three to 5 weeks are required
for antibody formation to have occurred.
2. [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae can be isolated on special media or in 5-7-day embryonating chicken eggs. Trachea, sinuses,
air sacs or synovial exudate are preferable for culture. The isolated [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma can be identified by direct
fluorescent antibody techniques applied to colony imprints. Alternatively, exudate may be inoculated into
the foot pad of chickens and turkeys to reproduce typical lesions. Later, their preinoculation and
convalescent sera may be tested against [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae antigen and [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum antigen. The HI test can
be used to confirm agglutination test results.
3. A commercial PCR test specific for [/FONT][/FONT][/FONT][/FONT][/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae is available. Tracheal swabs from a number of birds can
be tested.
4. Synovitis must be differentiated from arthritis caused by [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Staphylococci, fowl typhoid, pullorum disease,
and viral arthritis. Agents of the first three are easily cultured. Viral arthritis should infect experimentally
inoculated chickens but not turkeys.
CONTROL
1. In most areas it is now possible to get chicks or poults that were hatched from eggs from MS- free flocks.
If possible, start with such chicks or poults.
2. Insofar as is possible, raise the birds in quarantine under the all-in, all-out system.
3. Synovitis can usually be prevented by continuously giving the birds a low-level antibiotic in the feed. This
is an expensive procedure. Many antibiotics used for treatment can be used for prevention but are fed at a
lower level.
4. Commercial [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae vaccine is available and maybe beneficial in certain management situations.
TREATMENT
Treatment of lame birds with well-established synovitis is usually not very satisfactory. Relatively high
levels of antibiotics are required and may be given in feed or water. Aureomycin and Terramycin have been widely
used. Streptomycin has been used intramuscularly in small groups of birds where they could be handled[/FONT][/FONT][/FONT][/FONT]​

individually.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
100
2. In later stages of the disease the birds may be emaciated or thin and there may be no lesions in internal
organs. Exudate in joints and tendon sheaths may be inspissated or joint surfaces may be stained orange or
yellow. Breast blisters often are present secondary to trauma from resting on the floor.
3. Respiratory lesions may be absent or consist of a mild mucoid tracheitis, airsacculitis, or sinusitis, lesions
that are usually associated with

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum infection (chronic respiratory disease). Such birds may
not have the usual lesions of synovitis described above.
DIAGNOSIS
1. Typical signs and gross lesions, especially epizootic lameness and characteristic exudate in swollen joints
or tendon sheaths, are suggestive of synovitis. The diagnosis can be strengthened by obtaining positive
plate agglutination tests for synovitis on sera from a few birds in the flock. Three to 5 weeks are required
for antibody formation to have occurred.
2. [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae can be isolated on special media or in 5-7-day embryonating chicken eggs. Trachea, sinuses,
air sacs or synovial exudate are preferable for culture. The isolated [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma can be identified by direct
fluorescent antibody techniques applied to colony imprints. Alternatively, exudate may be inoculated into
the foot pad of chickens and turkeys to reproduce typical lesions. Later, their preinoculation and
convalescent sera may be tested against [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae antigen and [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum antigen. The HI test can
be used to confirm agglutination test results.
3. A commercial PCR test specific for [/FONT][/FONT][/FONT][/FONT][/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae is available. Tracheal swabs from a number of birds can
be tested.
4. Synovitis must be differentiated from arthritis caused by [/FONT][/FONT][/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Staphylococci, fowl typhoid, pullorum disease,
and viral arthritis. Agents of the first three are easily cultured. Viral arthritis should infect experimentally
inoculated chickens but not turkeys.
CONTROL
1. In most areas it is now possible to get chicks or poults that were hatched from eggs from MS- free flocks.
If possible, start with such chicks or poults.
2. Insofar as is possible, raise the birds in quarantine under the all-in, all-out system.
3. Synovitis can usually be prevented by continuously giving the birds a low-level antibiotic in the feed. This
is an expensive procedure. Many antibiotics used for treatment can be used for prevention but are fed at a
lower level.
4. Commercial [/FONT][/FONT]

[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]M. [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae vaccine is available and maybe beneficial in certain management situations.
TREATMENT
Treatment of lame birds with well-established synovitis is usually not very satisfactory. Relatively high
levels of antibiotics are required and may be given in feed or water. Aureomycin and Terramycin have been widely
used. Streptomycin has been used intramuscularly in small groups of birds where they could be handled[/FONT][/FONT][/FONT][/FONT]​

individually.

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]MYCOPLASMOSIS[/FONT][/FONT]
101
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]THE MYCOPLASMOSES[/FONT][/FONT]

[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]A[/FONT][/FONT]
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]Name(s) of the Disease[/FONT][/FONT]
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]Etiologic Agent[/FONT][/FONT]
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]Nature of the Disease[/FONT][/FONT]
[FONT=TimesNewRoman,Bold][FONT=TimesNewRoman,Bold]Major Lesions[/FONT][/FONT]
Chronic respiratory disease
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma[/FONT][/FONT]
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum[/FONT][/FONT]
A respiratory disease.
Airsacculitis, adhesive pericarditis, fibrinous
perihepatitis. Occasionally causes synovitis or
salpingitis.
Infectious sinusitis
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma[/FONT][/FONT]
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]gallisepticum[/FONT][/FONT]
Unilateral or bilateral sinusitis. May spread
to or occur initially in the lower respiratory
system.
Swollen infraorbital sinus (es) may or may not
be followed by airsacculitis, pericarditis, and
perihepatitis.
Infectious synovitis
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma[/FONT][/FONT]
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]synoviae[/FONT][/FONT]
Involves synovial lining of joints, tendon
sheaths. Results in lameness, debility.
Swollen joints and tendon sheaths. Feet, shanks,
hocks more obviously affected. Occasionally
causes airsacculitis in broilers and turkeys.
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma meleagridis[/FONT][/FONT]
infection; MM
infection
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma[/FONT][/FONT]
[FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]meleagridis[/FONT][/FONT]
A venereal infection of
turkeys, usually transmitted by infected
pooled semen. Produces airsacculitis in
many progeny.
Airsacculitis in nonhatching or newly hatched
poults. May spread laterally to other young
poults as an airsacculitis. May lead to
airsacculitis in market birds.​

A

More than 20 serotypes of [FONT=TimesNewRoman,Italic][FONT=TimesNewRoman,Italic]Mycoplasma have been identified in chickens, turkeys, and ducks. These three are the most significant pathogens.


[/FONT][/FONT]

 

[casportpony]

Well for her sake, I hope she goes peacefully in her sleep. I know that not easy for us to see, but I've read stories of birds having a spasm freak out thing. I'd much rather peaceful. How long have you been dealing with MD?

Deb

Well, she died, knew she would as thin as she was. Don't feel bad for me, I'm getting used to it and quite feeling quite numb to deaths in my flock.

It's not that I don't care, heck, I tube feed them until they start to shut down, I just don't cry anymore.

Anyway, had the occasional Marek's in my flock since about 2003, but 2012 was the first time I sent one off for necropsy and it was then I learned about all of the different forms. Before then, I always thought it was one foot forward, one back... Silly me!

-Kathy

 

[casportpony]

FWIW, the lab I work with said that they would like for people to send a blood sample (from before euthanasia/death) from their bird when they send in the carcass. Of course that means that one has to learn how to do their own blood draws, which is on my list of things to learn. They said that it would make testing for MS and MG much easier for them.

-Kathy