VMPM 7437 Ruminants, Mastitis, Avian (Unit 4)

Contagious Pustular Dermatitis Etiology

Parapoxvirus → at least 6 different “strains”

Also known as Orf, contagious ecthyma, sore mouth and many other names

Contagious Pustular Dermatitis Epidemiology

Found worldwide in sheep and goat populations - ZOONOTIC

Transmitted via contact with scabs, exposure to contaminated facilities

Very stable virus, once a facility is contaminated often considered contaminated indefinitely

• Especially wood and interior areas

Contagious Pustular Dermatitis Clinical Signs

• Often 100% morbidity, low mortality

  • Endemic herds, youngstock only

• Scab-like lesions at mucocutaneous junctions

  • Lips

  • Oral cavity

  • Teats and udder

    • From nursing of affected lambs/kids

    • Very painful → refusal to allow nursing

    • Predispose to mastitis

• Typical 2-3 week course of visible clinical disease

  • 3-14 day incubation period followed by:

    • Papules → vesicles → pustules → scabs

  • Scabs heal and drop off in 1-4 wks

Rare potential for severe disease that persists or extends to respiratory or GI tracts

Humans – painful lesions

Contagious Pustular Dermatitis Diagnosis

Typically based on clinical signs

• Bluetongue is a potential differential

• FMD, sheep pox are FADs that could look similar at certain stages

Electron microscopy, PCR

• Available from some VDLs

Contagious Pustular Dermatitis Treatment

Typically not necessary as infection is usually self-limiting

• Use of topical ointments or astringents may actually delay healing

Neonates may require supplemental feedings, particularly if teat sores are concurrently present

Secondary bacterial infections can be treated with topical or systemic antibiotics

• Gram positive skin infections (Staph sp)

• Pneumonia

Contagious Pustular Dermatitis Prevention and Control

Quarantine and examine all animals entering farm

Avoid contact with shared feeders, waterers, trailers, grooming supplies at shows or sales

Isolate affected animals during outbreaks to prevent spread to naïve animals

Vaccination

• LIVE VIRUS VACCINE available in US (ovine)

• DO NOT USE IF VIRUS IS NOT ALREADY PRESENT ON FARM

• ZOONOTIC RISK

• Scarification of wool/hair free area followed by application of virus

Ringworm/Club Lamb Fungus Etiology

Trichophyton verrucosum, occasionally T. mentagrophytes ZOONOTIC

Ringworm/Club Lamb Fungus Epidemiology

Infected animals contaminate facilities and equipment, perpetuates in herd

Animals that are housed indoors, in winter most affected

Sheep that go to shows (club lambs) are clipped and bathed regularly

• Removes protective lanolin

• Creates small wounds that can serve as entry point for organism

Ringworm/Club Lamb Fungus Clinical Signs

Thick, scaly round spots that can become ulcerated or crust over

Spontaneous recovery typically in 8-16 weeks

Ringworm/Club Lamb Fungus Diagnosis

Clinical signs are highly suggestive

• Treat as if positive until proven otherwise

• Differentials:

  • Dermatophilosis, external parasites, zinc deficiency Staphylococcal dermatitis

Fungal culture (DTM)

KOH prep

Ringworm/Club Lamb Fungus Treatment

Sunshine + time

All treatments are extralabel and withdrawal times are rarely known so should be used with caution.

• Thiabendazole is probably the best product legally as there are veterinary products available; recently sold and not all products may still be available.

• Fulvicin (griseofulvan; human antifungal) (10mg/kg) is effective but is extra label. No data on withdrawal times have been published.

• Over the counter human products like Tinactin (tonaftate antifungal) have also been used.

• Captan (plant fungicide). Has been used topically by mixing with water to make a paste. No withdrawal time has been published and one needs to wear gloves and be careful with the Captan. NOT CURRENTLY RECOMMENDED – EPA product, no extralabel use!!

Ringworm/Club Lamb Fungus Prevention and Control

Isolate affected animals to prevent spread, disease is self-limiting in most cases

Do not allow animals with lesions to attend shows and events!

Sanitize equipment between animals/farms

Do not share grooming equipment at shows and events!

Pediculosis (lice) Etiology

Bloodsucking (Linognathus sp. Solenopotes sp. Haematopinus sp.)

Chewing or biting (Bovicola [formerly Damalinia] sp.

Most are host specific, so unique species of each effect cattle/goats >> sheep

Pediculosis (lice) Epidemiology

Obligate ectoparasites

Most transmission is through direct contact, limited survival in environment and on grooming supplies, etc

Pediculosis (lice) Clinical Signs

Pruritus with a rough, shaggy hair coat, +/- weight loss, decreased production efficiency

Sucking lice may cause anemia, hypoproteinemia, and death – especially when combined with intestinal parasitism

Most commonly observed in late winter

Pediculosis (lice) Diagnosis

Visible via the naked eye

Collection and viewing under a microscope allows determination of sucking vs biting species which can be important for directing therapy

Pediculosis (lice) Treatment and Prevention

Treatment of entire herd with EPA approved insecticide (no extralabel use allowed) for chewing and bloodsucking lice

• Most treatments are not ovicidal and thus treatment should be repeated in at least twice in 2-week intervals.

• Exception: Clean-up II with IGR

Bloodsucking lice can be treated with injectable deworming products such as the avermectins

Treatment and isolation of new herd additions will prevent herd entry

Mange Etiology

Chorioptic mange: Chorioptes bovis/ovis/caprae – most common mange mite in US; host specific

Psoroptic mange: Psoroptes ovis (cattle); Psoroptes cuniculi (goats, sheep), P. communis var ovis (sheep) - rare, reportable in US; host specific

Demodectic mange: Demodex caprae/ovis – may be common, mostly immunocompromised

Sarcoptic mange: Sarcoptes scabiei var bovis/ovis/caprae – reportable, zoonotic

Mange Epidemiology

Transmission occurs through direct contact or indirectly through contact with equipment or grooming tools

Mange Clinical Signs

Pruritus, crusting, self-trauma and alopecia

Different types have different preferred patterns:

• Chorioptic mange tends to affect the hindlimbs, lower, limbs, scrotum and abdomen

• Psoroptic mange tends to affect the back and flanks of cattle, trunk in sheep and ears in goats.

• Demodectic mange tends to affect the face, shoulders and trunk

Mange Diagnosis

Skin scrapings viewed under a microscope are necessary for diagnosis

Mange Treatment and Prevention

Treatment of entire herd with injectable or topical deworming products such as the avermectins, repeated in at least twice in 2 week intervals

Lime sulfur and other (coumaphos, toxaphene, phosmet) dips, caution with establishing withdrawal times

Treatment and isolation of new herd additions will prevent herd entry

Foot and Mouth Disease

Cattle	Swine	Sheep/Goats
Disease Indicators	Amplifying Host	Maintenance Host
Often first species to show signs	Produce large amounts of aerosolized virus
Can carry the virus for up to 6 months Some animals may remain infected for up to 3-1/2 years	Rare, possibly carry the virus up to  28 days	Can carry/shed the virus for up to 4 months for goats and 12 months for sheep

FMDV carriers are defined as animals in which the virus can be found for more than 28 days after infection. Animals can become carriers whether or not they had clinical signs. How long an animal can remain a carrier of the virus varies with the species. Most cattle carry FMDV for six months or less, but some can remain persistently infected for up to 3.5 years. Cattle are considered indicator hosts because they are often the first species to demonstrate clinical signs. Pigs are not thought to become carriers; however, they are considered amplifying hosts, as they produce large amounts of aerosolized virus. The virus is shed for a short time and swine are not considered long-term carriers; there have been a few reports documenting the presence of viral nucleic acids after 28 days. Sheep and goats are considered maintenance hosts and may shed the virus for up to 12 months in sheep and up to 4 months in goats.

Foot and Mouth Disease DDx in ruminants

DDX for Foot and Mouth disease in ruminants:

• Vesicular stomatitis

• Malignant catarrhal fever (cattle only)

• Infectious bovine rhinotracheitis (cattle only)

• BVD mucosal disease (cattle > sheep/goats)

• Bluetongue (sheep/goats > cattle)

  • Epizootic hemorrhagic disease (cattle)

• Contagious pustular dermatitis/contagious ecthyma (sheep/goats)

• Bovine papular stomatitis

• Rinderpest (eradicated)

New World Screwworm Etiology

Cochliomyia hominivorax

New World Screwworm Epidemiology

Can affect all warm-blooded animals

Previously present in the US (pre-1970), eradicated through extensive control efforts including a permanent sterile fly barrier established between Panama and Columbia.

• Recently paused and moved north into Mexico

An outbreak occurred in the Florida Keys (Key deer) in 2016 but was quickly eradicated.

Recently has been identified within 400 miles of Texas in Mexico prompting closure of US:Mexican border to all livestock as of May 2025.

New World Screwworm Clinical Signs

Flies are attracted to wounds.

Animals that have recently given birth or were born, been injured or had a surgical procedure (castration, dehorning, branding) are most at risk.

The fly larvae (maggots) burrow into the living tissue causing very painful lesions (myiasis) that can lead to fatal outcomes.

New World Screwworm Diagnosis

Identification of maggots in wounds or other body openings, especially wounds with bloody discharge, foul odor, and those that become deeper and larger overtime.

Adult screwworm flies are about the size of a common housefly (or slightly larger).

Orange eyes, a metallic blue or green body, and three dark stripes along their backs.

Flies, eggs, and maggots are collected and placed in 70% alcohol for identification.

New World Screwworm Treatment

Clean affected area and remove all visible larvae; apply topical antiseptics to treat secondary infections.

Apply topical or systemic antiparasitic treatments to kill remaining larvae.

• F10 Antiseptic Wound Spray with Insecticide (benzalkonium chloride, polyhexanide, cypermethrin) – EUA for prevention and treatment

• Exzolt Cattle-CA1 topical solution (fluralaner) – conditional approval (also for cattle fever tick) for prevention and treatment

• Ivermectin injectable (OTC) – EUA for prevention

New World Screwworm Prevention

Sterile fly eradication program – female flies mate only once, so breeding to sterile males slowly leads to eradication.

Rinderpest Etiology

Morbilivirus, closely related to measles, canine distemper, PPR

Rinderpest Epidemiology

ERADICATED!!

Considered the deadliest disease of cattle in history

WOAH-listed disease – must be reported

Previously endemic in Africa, Asia, with frequent devastating outbreaks in Europe

Rinderpest Clinical Signs

Explosive outbreaks with whole herds affected

Four “Ds” = depression, dehydration, discharge, diarrhea

Necrosis and erosions of the GI and upper respiratory tracts

Death in European breeds

Some native breeds more resistant

Rinderpest Diagnosis

Serology, RT-PCR

Rinderpest Prevention

Eradication was achieved because:

• Transmission required close contact, did not persist in environment

  • No carrier state

• High quality vaccine (live attenuated) with life-long immunity

  • Heat stable, did not require cold chain

  • No longer in use

• Effective diagnostic assays

• Global effort including strict quarantine and movement controls

Contagious Bovine Pleuropneumonia Etiology

Mycoplasma mycoides subspecies mycoides small colony

Contagious Bovine Pleuropneumonia Epidemiology

Endemic with frequent outbreaks in sub-Saharan Africa; also Asia, India

Eradicated from North America, Europe, Austrailia

The organism is highly contagious and is spread by inhalation of droplets coughed up by infected cattle

About 25% of recovered cattle become chronic carriers of the organism which are difficult to detect in an infected herd

Transplacental transmission can occur

Contagious Bovine Pleuropneumonia Clinical Signs

Rapid disease progression with very painful, difficult breathing (usually rapid and shallow), fever up to 107 F

Some animals will become recumbent and die within 1-3 weeks.

Marbled appearance of the lungs due to thickening of the interlobular septa; fluid (up to 10 L) in the thoracic cavity; thick layer of fibrin.

Contagious Bovine Pleuropneumonia Diagnosis

Serology (CFT, cELISA) – often used for international trade

PCR, Culture

Contagious Bovine Pleuropneumonia Treatment

WOAH (OIE) reportable disease. Slaughter of all infected and exposed animals (was used to eliminate from the US).

In endemic areas, macrolides and fluoroquinolones are reported to be effective. Treated animals may remain carriers.

Contagious Bovine Pleuropneumonia Prevention and Control

Vaccination (attenuated live – T1/44 strain) is practiced in endemic areas.

Trade restrictions for endemic regions

Trypanosomiasis Etiology

Cattle, sheep, and goats are infected, in order of importance, by Trypanosoma congolense, T. vivax, and T. brucei brucei.

T. brucei rhodesiense and T brucei gambiense are zoonotic, with people as the predominant host.

Trypanosomiasis Epidemiology

Group of protozoal diseases transmitted by tsetse flies, “sleeping sickness”

Tsetse flies are restricted to Africa, and several different species exist with specific geographic range and preferred mammals on which to feed.

Some mechanical transmission also occurs through other biting flies, especially outside tsetse-endemic areas such as in Central and South America.

Trypanosomiasis Clinical Signs

Localized skin infections (chancres) occurs at the location of the tsetse bite; the incubation period is typically 1-4 weeks.

Primary clinical signs include intermittent fever, weight loss, enlarged lymph nodes, diarrhea and anemia.

Chronic disease often leads to high mortality especially if poor nutrition or stress is present.

Trypanosomiasis Diagnosis

Demonstration of trypanosomes in stained blood smears.

Serology; PCR also possible but not commonly available in endemic areas.

Trypanosomiasis Treatment

In endemic areas, diminazine aceturate or homidium bromide can be curative

Trypanosomiasis Prevention and Control

Breeding of cattle breeds with innate resistance (indigenous West African breeds)

Control of tsetse flies (sprays, dips), sterile fly release

Prophylactic treatment

Peste Des Petits Ruminants (PPR) Etiology

Morbilivirus, closely related to Rinderpest (eradicated)

PPR Epidemiology

WOAH-listed disease – must be reported

Africa, Middle East, Turkey, Asia, India

Recent outbreaks in eastern Europe (2024-current)

• Hungary* (back to free)

• Croatia, Romania, Greece (no longer free)

• Kosovo, Albania

Vietnam – October 2025

Transmission occurs rapidly via airborne droplets or direct contact, or contact with contaminated environments

Explosive outbreaks, 2-6 days incubation

PPR Clinical Signs

Targets lymphoid tissue and epithelial lining of intestines

High fever, depression, mucopurulent ocular and nasal discharge

Extensive erosions of oral/pharyngeal mucosa, enteric lesions (“zebra stripes), profuse diarrhea

Asymptomatic possible but rare

PPR Diagnosis

Clinical signs and post-mortem findings highly suggestive

Antigen capture ELISA, PCR, IHC all possible to ID

Serology also used

• Can’t differentiate between Rinderpest

• Useful in vaccination/eradication programs

PPR Treatment and Prevention

Non-endemic areas:

• Import restrictions from endemic areas

• Rapid reporting to animal health officials

• Quarantine of affected animals

• Test and culling of any affected or exposed animals or total depopulation may be required

Endemic areas

• Vaccination is used to control disease

FAO/WOAH Eradication goal by 2030

• Only 1 serotype

• No carrier state or reservoir outside of domestic small ruminants

• High quality vaccine with life-long immunity

  • Requires cold chain

  • Goal of 100% vaccination of >3mo old, 70% herd immunity

• Effective diagnostic assays

Contagious Caprine Pleuropneumonia (CCPP) Etiology

Mycoplasma capricolum subsp. capripneumoniae

CCPP Epidemiology

WOAH-listed disease – must be reported

Occurs in Africa, Asia, Middle East

Has never been reported in North or South America

Goats >> sheep

Wild ruminants?

Transmission occurs rapidly via airborne droplets or direct contact, or contact with contaminated environments

Explosive outbreaks, 6-10 days incubation

CCPP Clinical Signs

Severe respiratory infection – coughing, dyspnea, frothy nasal discharge

High fever, depression, anorexia

Up to 80% mortality

Survivors have chronic cough, nasal discharge, debilitation

CCPP Diagnosis

Severe lung lesions present on necropsy

• Serofibrinous pleuropneumonia

• Consolidated, hepatized lung

  • Granular texture

Culture can be challenging

PCR, IHC preferred

Serologic testing to identify chronic disease

CCPP Treatment and Prevention

Antibiotic therapy as for typical Mycoplasma infections can be effective but may not eliminate carrier status

Supportive care, most acute cases die

Non-endemic areas:

• Import restrictions from endemic areas

• Rapid reporting to animal health officials

• Quarantine of affected animals

• Test and culling of any affected or exposed animals or total depopulation may be required

Endemic areas

• Vaccination is used to control disease

Mastitis

• A disease with a high component of management

• Cost $13 billion worldwide

• U.S. Importance

  • Over $2 billion annually

  • Thought to be the most costly problem in the dairy industry

Cost of clinical vs. subclinical mastitis

Culling Decisions

• Approximately 25% of all culls leave the herd in the first 60 days of lactation

• Cows tend to become invisible until they get sick or are culled for low production

• True cause for low production may not be discerned and/or recorded

• Adequate bunk space, nutrition, sanitation, cow comfort, proper body condition, etc. all play a role in cow longevity

Mastitis Severity Scores: Better System for Records?

1. Milk is abnormal

2. Milk and udder are abnormal

3. Cow is sick with mastitis

Dairy Herd Improvement Association (DHIA) → records “Times Severe” on records

Importance of Mastitis

• Loss of production

• Loss of financial incentives

  • Poor quality milk (high leukocyte counts)

• Animal Welfare

  • Painful condition

  • Toxic mastitis and down cows

Nonspecific Mammary Gland Defense Mechanisms

• Anatomical

  • Smooth muscle → surrounds the teat duct

  • Keratin → forms a plug

    • Some high producing cows do not form a good keratin plug

    • Contains bactericidal fatty acids

    • Defensins

    • Also can harbor bacteria

• Milk flow

  • Flushes out pathogens and toxins

  • Incomplete milk-out can lead to mastitis

• Milk leukocytes

  • Highest in foremilk and stripping milk

  • Neutrophils → predominant cell in infection

    • Killing function → Inhibited by fat globules (butterfat)

    • Milk neutrophil ingested fat droplets

    • Neutrophil inability to function well in milk

      • Lack of glucose (lactose is the main milk sugar)

      • Decreased glycogen

      • Deficiency of opsonins (complement and antibody)

        

• Nonspecific soluble factors

  • Lysozyme

    • Breaks down bacterial peptidoglycan

    • Active only against Gram positives

    • Low in normal milk

    • Increases during infection

  • Lactoferrin

    • Chelates iron needed by bacteria

    • Low in normal milk

    • High in non-lactating (involuted) gland

  • Defensins

    • Antibacterial proteins

    • Produced by a variety of cells (epithelial and neutrophils are especially good producers)

• Involution

  • 365 days in a year, 305 days in an average lactation, 60 days of dry period

  • Reason for dry period: allow regeneration of mammary epithelium

  • Should aim for 45-60 days

  • Involution occurs usually in the first 2 weeks of the dry period. Common time for new infections

  • 

• Diet

Keratin in streak canal, Smooth muscle

Keratin plug forms in streak canal

Milk Production at Dry-Off

• National Mastitis Council recommends that cows be producing 33 lbs or less of milk per day at dry-off

• Hard to do in high producing herds

• Minnesota average at dry-off is about 60 lbs per day

• Cows are more susceptible to environmental mastitis first two weeks

• Keratin plug formation can be delayed due to leakage

• Cows are uncomfortable due to engorgement of udder

Specific Mammary Immune Mechanisms

• Humoral Immunity

  • IgG1 Predominant in normal milk

    • Opsonic for macrophages

    • Not opsonic for neutrophils

    • Can fulfill some of the functions of IgA

  • IgG2 Opsonic for neutrophils

  • IgA may act to:

    • Prevent adherence to mammary epithelium

    • Neutralize toxins

    • Agglutinate bacteria

    • Prevent multiplication of bacteria

  • IgM

    • Good at fixing complement

    • Antibody concentrations are low in normal milk

• Cell-Mediated immunity

  • CD8+ T-cells attack cells that are infected

  • Seen with some viral infections and some chronic bacterial infections

  • Influx of mononuclear cells into the mammary gland: not so good

    • Obliteration of functional secretory tissue

    • HPAI causes fibrosis of mammary tissues

Bovine Immunoglobulin mg/ml

Immunization:

• Stimulate antibody production

• Stimulate cell-mediated immunity

Bottom Line to Prevent Mastitis

• Maintenance of anatomical integrity

• Clean environment to lessen exposure

• Maintenance of good milk flow to “wash out” bacteria and toxins

• Use of the few good vaccines

• Good milking techniques/equipment

Many Different Species and Breeds of Poultry and Game Birds

• Hobby flocks are becoming more common but HPAI has dampened enthusiasm

• Some are adaptable to urban lifestyles

• Species and different breeds may have different diseases affecting them

• Commercial flocks may be free of certain diseases and hobby flocks???

• All-in All-out vs Mixed age

• Free-range vs barn-raised vs cage-raised

• Straight run (half egg layers, half males) vs. sexed

Broiler vs. Breeder and Laying Chickens

Broilers

• Chickens harvested at 5-7 weeks of age

• Turkeys 14-18 weeks of age

Breeders and Egg layers

• Start laying eggs about 18 weeks of age

• Vaccinations should be completed 4-8 weeks prior to start of egg laying if using MLV

Immunization Issues

• Available vaccines are often sold in units of 1000 to 10,000 doses

• Vaccination in-ovo and as day-old chicks may be the only immunizations received in hobby flocks

• Vaccinations through water or mist/aerosol are common

• Vaccination and revaccination may not be practical for hobby producers

• Short lifespans in broiler chickens

  • Immunization in-ovo or not at all with some pathogens

  • Immunize hens for antibody in eggs

• Wing web vaccination

• Eye drop vaccination- drains through nasolacrimal duct into mouth and stains mouth blue to indicate proper vaccination

Unique Drug Problems

Drug residues in eggs

• Similarities to milk residues

• All antibiotics approved for use in laying hens must have a zero-day withdrawal

Treatment of Game Birds

• Chickens and turkeys are considered major species by the FDA/CVM

• All other avian species are considered to be minor species

• There are very few drugs approved for minor avian species

• Guidance 615.115

  • Not a law, AMDUCA is law

  • Major species: cattle, swine, chickens, turkeys, horses, dogs, cats

  • Provides regulatory discretion for veterinarians to use feed or water for delivery to alleviate pain and suffereing due to diseases

  • Minor Species extra-label drug feed use

  • Must be no approved drug that will work

  • Feed use of the drug must be approved in a major species

  • Feed must be labeled on the VFD for dose and duration identical to the major species label

  • Limited to farmed or confined minor species (not wild)

  • Must have valid VFD: veterinarians are liable for problems that occur

  • Therapeutic use only (no production drugs)

  • Use in mammals limited to drugs approved in a mammal species

  • Use in avians limited to drugs approved in an avian species

  • Aquaculture drugs have to be approved in an aquatic species

ILHAC Priorities

• All Poultry

  • Avian Influenza infections – Low Path Avian Influenza (LPAI) and High Path Avian Influenza (HPAI) epidemiology, prevention and control, research to identify routes of infection.

  • Antimicrobial resistance and antibiotic substitutes in poultry production

  • Vaccine Availability and application: one vaccine versus two killed injections

  • Animal well-being

• Turkeys

  • Reovirus

  • Clostridium - Dermatitis

  • ORT (Ornithobacterium rhinotracheale)

• Layers and Broilers

  • E. coli Peritonitis (#1 disease concern of veterinarians in egg production)

  • Infectious Coryza (Avibacterium paragallinarum)

  • Clostridial infection: necrotic enteritis and Focal Duodenal Necrosis (FDN)

  • Food Safety - Salmonella spp. (Salmonella Enteritidis)

  • Internal Parasites – including Coccidia and round worms. It is believed these challenges will only become greater with the increased prevalence of Cage-free production. At the present time, there are no treatments available?

  • Campylobacter hepatitis and Spotty Liver Syndrome - lack of real-time PCR for diagnosis

  • Erysipelas and Pasteurella multocida

  • Enterococcus septicemia, inclusion body hepatitis are growing concerns in broilers and broiler breeders.

Cannibalism

• Chickens, turkeys and some others are omnivores

• Dead birds can serve as sources of disease organisms

• Need to remove dead birds promptly

• Birds can get buried in litter

• Discovered later and consumed

• Can serve as source of Erysipelas, botulism, necrotic dermatitis

White Leghorn

Male leghorn chicks are euthanized ASAP after hatching

Brown Egg Layers

Plymouth Rock, Orpington, RI Red

Cornish Cross

Meat breed, very rapid growth

Poultry Litter Conditions

• More important for broilers or cage-free egg layers

• Complete clean-out may occur once a year or less often in commercial facilities

• Partial clean-out between batches

• Dust: dry conditions, respiratory disease

• Ammonia: wet bedding, respiratory disease

• Mold

• Pathogenic organisms: bacteria, viruses, fungi

• Poor litter condition leads to burnt hock syndrome and foot lesions

Litter Moisture

Litter needs to be friable and dry and clean

• Air change rate: probably the most important

• Litter material and depth (don’t want them on concrete/dirt)

• Drinker design (leaking, wet bedding)

• Stocking density (as they get bigger, make sure there is enough space)

• Diet (too much fat in diet can lead to greasy bedding)

• Flock health

Lymphoid Leukosis/Sarcoma

• Avian leukosis virus (retrovirus)

• Subgroups A, B, C, D, E, and J

• Classically only important in chickens, some disease in game birds

• Previously widespread in virtually all chicken flocks except SPF (specific pathogen free) flocks

• Infrequent or absent in some large commercial flocks due to eradication efforts since the 1980s. Currently more of a problem in broilers (J subgroup with myeloid tumors)

• Tumor mortality is <4% with occasionally higher numbers

Lymphoid Leukosis Epidemiology

• Infected hens shed virus into albumen or yolk

• Congenitally infected chicks usually remain viremic for life

• Most virus spread is horizontal early in life

• Once eliminated from breeder hens, it is relatively easy to maintain virus-free flocks

• Most commercial chickens have been selected for genetic resistance

Tumors

• Most of the economic loss is due to decreased egg production rather than tumors

• Usually 16 weeks of age or older

• Most tumors result from induction of bursal cells

• Apparently a wide variety of tumor types can be associated with these viruses

  • Lymphoid is most common

  • Non-lymphoid tumors are dependent on strain of virus, strain of chicken, age of exposure, dose, and route of infection

Lymphoid Leukosis Diagnosis

• Demonstration of the virus is not helpful unless the virus is supposed to be eradicated from a group of chickens

• Gross and microscopic characteristics of the tumors

  • Liver, spleen, other organs

  • Bursal tumors are almost pathognomonic

  • No peripheral nerve lesions

    • Helps differentiate from Marek’s

Bursa of Fabricius near cloaca

Control/Eradication of Leukosis

• Test eggs from breeder flocks for viral antigen

• Discard eggs from positive hens.

• Rear breeder hens in small groups to limit the possibility of having an infected hen

• Grow genetically resistant strains of hens.

• Immunization has not been successful.

• Most commercial chickens are infected.

Marek’s Disease

Alphaherpesvirus with lymphotrophic properties of gammaherpesvirus

One of the most ubiquitous infections in chickens

• Infects feather follicles: Results in high concentrations in dust and litter of poultry houses

• Highly contagious: Once in a barn, all chickens get infected

Not usually a problem in turkeys

Different Marek’s Disease Viruses

• Gallid Herpesvirus 2 (MDV1, Virulent for chickens)

• Gallid herpesvirus 3: (MDV2, Avirulent for chickens)

• Meleagrid Herpesvirus 1 (turkey Herpesvirus) MDV3: Avirulent

Gallid Herpesvirus 2 (MDV1)

Further subdivided

• M= Mild

• V= Virulent

• VV= Very Virulent

• VV+ = Very Virulent Plus

VV+ viruses are the most common now

• Thought to be a result of routine immunization

Marek’s Disease

Subclinical disease can cause decreased growth rate and egg production

Lymphoid neoplasms

Others:

• Transient paralysis (range paralysis), early mortality syndrome, cytolytic infection, atherosclerosis and persistent neurologic disease

Marek’s Diagnosis

• Enlarged nerves

  • Most consistent gross lesion

  • Paralysis or paresis

• Enlarged feather follicles

  • Skin leukosis

  • Seen in broilers after defeathering

  • Cause for condemnation

• Lymphoid tumors in viscera

• Bursa usually not affected (unlike leukosis)

Marek’s on right: rough iris border, left eye normal

Paralysis from Marek’s Disease

Enlarged sciatic nerves

Tumors

Skin leukosis

Marek’s Control

• Strict sanitation: Delays infection until chicks are older.

  • Once in a poultry barn, it transmits readily via feather dust, etc.

  • Virus can survive for months in poultry house litter and dust.

  • Can inactivate virus in 2 weeks with high humidity and 37.5 C temp (100F):

  • Cleaning and disinfection can delay transmission or lower the infectious dose

• Genetic resistance of some chicken strains

Marek’s Vaccination

• Immunize initially with turkey virus or a combination of one or more other “avirulent” strains. Also have recombinants.

• In-ovo immunization at 17 to 19 days of incubation has been automated and used especially in the broiler industry.

• Re-immunize with a more virulent vaccine virus

  • Needed to protect against the vv+ viruses that are the most common in the industry

• Vaccine “leakage”

Avian Tuberculosis

• Mycobacterium avium subspecies avium

  • Serotypes 1, 2, 3 most commonly.

• M. genavense is common in pet birds

  • Most common in parrots but occasionally found in other species

• Transmission

  • Oral and aerosol (from feces) transmission

  • Natural habitats in soil and bird intestines

• Commercial poultry do not usually live long enough to develop disease unless in multi-age layer or breeder flocks.

• Backyard flocks, pet birds may develop disease

Avian Tuberculosis Epidemiology

• Forms tubercles or ulcerated lesions in the intestine which shed high numbers into the droppings.

• Organisms are usually ingested or inhaled from fecal material or other sources.

  • Dust

  • Soil

  • Fomites

  • Wild birds

Avian Tuberculosis Clinical Signs and Lesions

• Domestic chickens and wild birds raised in captivity are most susceptible.

• Emaciation, depression, diarrhea, marked atrophy of breast muscles

• Tubercles in multiple organs usually beginning with intestine and liver

• Usually no lung lesions

• Diagnose with culture of tissues or feces

• Acid-fast organisms on histopath

Avian Tubercles

Tubercles in liver and spleen

Tubercles in a chicken liver

Diagnosis and Prevention of Tuberculosis

• Tuberculin testing commercial birds in the wattle

• Whole blood agglutination for imported birds, waterfowl and others. Can read the reactions in minutes.

• Good biosecurity

Infectious Laryngotracheitis

• Gallid Herpesvirus 1

• Virulent strains and low virulence strains

• Life-long infection

• Recrudescence when stressed

ILTV

• Acute, highly contagious

• Affects mostly chickens and pheasants

• Usually 14 weeks of age or older (maternal antibody present up until then)

• Dyspnea

• Coughing with bloody discharge

  • Up to 50% mortality

• Subacute and subclinical forms occur

• Reduced egg production

Lesions of ILTV

• Acute disease

  • Necrotizing tracheitis

  • Blood, mucus, caseous exudates or hollow caseous casts in the trachea

  • Conjunctivitis

  • Swelling of infraorbital sinuses

• Subacute disease

  • Punctiform hemorrhages in the trachea and larynx

  • Low virulence vaccine strains can spread to non-immune birds

ILTV casts in the trachea and swollen sinus

ILTV Diagnosis

Intranuclear inclusions in tracheal epithelium early in the disease

PCR

Virus isolation

ILTV Control and Prevention

Good biosecurity

Virus remains viable 8-10 days in droppings but longer in winter temperatures

Remains viable up to 80 days in a carcass

ILTV Immunization

Endemic areas

• Live attenuated

  • Eye drop, water or spray

• Recombinant vector vaccines

  • In-ovo, subcutaneous and wing web

  • Fowl pox and Turkey herpesvirus recombinants

Newcastle Disease

• One of the most important diseases worldwide

• Avian Paramyxovirus 1

• Terms:

  • Velogenic viruses: Pathogenic to all ages of birds.

  • Mesogenic: Highly pathogenic for embryonic stages. Less severe in immature and older birds.

  • Lentogenic: Low virulence viruses, loNDV, can be used as vaccines

Virulent Newcastle Disease (vND)

Velogenic and mesogenic viruses are now referred to as vNDV

Other terms:

• Exotic Newcastle Disease (END)

• Velogenic ND (VND)

• Viscerotrophic velogenic ND (VVND)

2018 vND Outbreak

• Hundreds of backyard flocks in California

• Once commercial flock