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Avian Tuberculosis
AKA Avian Mycobacteriosis
M. avium (most common), M. intracellularle, {M. genavense} and others
MA or MAI complex (MAC, MAIC)= Mycobacterium avium-intracellularle infection in humans or birds
Avian TB
Pet birds, poultry, captive & free-range wild birds
All orders
Esp Anseriformes (ducks & geese), Gruiformes (cranes) & Galliformes (chicken-types)
In CAPTUVE collections!
NOT Zoonotic? Shared?
Young children & immunocompromised adults get it!
Probably from environment, not birds
Avian Tb Cont.
Transmission- thru feces (fecal-oral) or environment
fecal-oral → esp. caged birds
Signs: emaciation, chronic wasting, +/- diarrhea, listlessness (not active), decreased egg production (poultry), swellings around eyes, rarely respiratory signs
Much more common in adult vs young birds
Role of Stress
Stress greatly increases susceptibility (rare to see non-stress_
Types of Stressors:
Malnutrition, overcrowding, drought, extreme temperatures, other infections, pinioning (wing tip removal)
drought: no water, dehydration, no vegetation
What is a saprophyte?
A. A student who cheats on an exam
B. A pathogenic organism
C. An organism living on dead or decaying organic matter
D. A disease transmissible from people to animals
Sources of MAI complex
Feces
Ubiquitous environmental saprophytes (animals that’s dead or rotting)
Surface water
Soil
Acidic
Moist (marshy or prone to flood)
High in organic matter (saprophyte)
Contaminated with feces
Which came 1st?
Are wild birds the source or the recipient? don’t know
Both wild and captive birds may be carriers
What is a carrier?
Carrier
Is infected with the agent, but shows no signs
Capable of transmitting to others
Types: True (Latent), Incubatory, Convalescent
True: never impacted by agent, infecting others
Incubatory: not yet clinically infected until incubation period is over, infecting others
Convalescent: recovered, can still pass to others
Importance of Avian TB
Economic
Disease in poultry & caged birds (& swine)
Cross reactions in other LS (to TB)
Loss of free-ranging colonies or species
18,500 flamingos died in 1993 on 2 Kenyan lakes
Cross Reaction
A type of False Positive reaction on a diagnostic test
May occur when the animal is exposed to a similar agent, was infected but has eliminated the infection (but retains antibodies), or when they are vaccinated against the agent
M. avian, M/ bovis
Ante-mortem (diagnosis, before death)
VERY difficult, esp in wild birds
Clinical finding → clues
Chronic wasting, death (either after months, or sudden), emaciation, lethargy, poo quality feathers, distended abdomen (liver swelling & fluid build-up), lameness, +/- diarrhea, occular, cutaneous, or subcutaneous granulomas
Normal carriers → insidious Dz
Subtle or sneaky (hidden)
Ante-mortem Dx Cont.
Captive: intradermal tuberculin test, blood tests, culture (dead animals)
Wild: none practical (fecal culture?)
false negatives
Poster-mortem Dx
Liver, spleen, intestines (best luck)
Many other organs less frequently involved
Granulomas (nodules), or diffuse inflammation
Enlargement (liver & spleen)
Muscular wasting
How assess? big, pectorals, keel: strength to flop wings
Definitive Dx
Necropsy (post-mortem): suggestive
Microscopic: more specific
Acid-fast bacteria (pretty certain)
Definitive: culture &/or molecular identification of MAI complex bacteria
Treatment
Rarely works
Euthanasia to prevent transmission
Control/Prevention
Captive: ID (intradermal tuberculin test) and remove infected birds, hygiene (remove feces & other contaminated material), avoid overcrowding (minimize stress), supply quality nutrition
Prevent contact with wild birds
Wild: Good Luck!
Prevent contact with domestic birds!
Johne’s Disease
Pronounced “Yo-Knees”
AKA Paratuberculosis
Mycobacterium avium subsp. paratuberculosis
Still considered part of the MAI complex
Usually abbrev. “MAP”
Johne’s (MAP)
Domestic: cattle, sheep, goats, farmed cervids
Wild: many susceptible species but rare
Bovine: bison, bighorn, Mt. goat, etc.
Cervids: WTD, MD, elk, Sika etc,
Camelids: Camels, llama, alpaca
Lagomorphs: rabbits
Primates:
Johne’s
Young animals more susceptible to infection
Mid-Old age animals more likely to show signs
Another chronic wasting disease!
Can take years!
Why might some people assume Johne’s is a disease of birds?
A. Dr. Johne was a famous ornithologist
B. The species name of the agent implies an avian host
C. The bacteria that causes Johne’s is airborne
D. Johne’s IS a disease of Birds!
Johne’s transmission
Fecal-oral
In utero-BHS
Environmental contamination occurs
Epidemiologic Triad (decided how severe an outbreak is going to be in a population)
Host- age, immunocompetence (individual animal)
Agent- strain virulence, pathogenicity, how it is transmitted, special features (spores)
Environment- degree of contamination, humidity, exposure to UV (sunlight) (destroys pathogens), stressors affect host
Johne’s 2
MAP survive in feces, soil & water: 1 year
Healthy Carriers may shed for years (host)
More problematic in Intensive LS operations (environmental)
Eradication nearly impossible, Control in LS very valuable
Johne’s Signs
Diarrhea
intermittent (recover, get again)
Chronic wasting
losing weight over months or years
keeping intestine from absorbing nutrients properly
animals don’t get enough protein
Hypoproteinemia → bottle jaw (fluid collected under jaw)
Abnormal antlers/horns
Fatal if clinical signs
IS Johne’s Zoonotic?
Does it cause Crohn’s Disease in humans?
If MAP- Crohn’s more likely
If Crohn’s, MAP more likely
Does this prove causation? no, association
What is the source of MAP?
Johne’s Dx
Signs & lesions= suggestive (emaciation, Diarrhea, thickened {granulomatous} intestines, colon)
LS-rectal scraping or biopsy with Acid-Fast bact= presumptive (diagnoses)
Definitive- culture (feces inc.)
Johne’s Treatment
None
Prevent introduction
Control in LS: Cull animals with signs, manure management, good husbandry
Johne’s control in wildlife
Most impractical or impossible
Increasing harvest to reduce density been tried- reduced, but not eliminate
Do not use for translocations!
Why translocate WL?
Taking WL from one area and moving to another
reestablish population
Inc. genetic diversity in big population
Can also lead to disease transmission
Johne’s in BHS
CO & WY
Behavior facilitates fecal-oral transmission
Point Reye’s National Seashore
Tule elk infected with MAP
Clinical Disease rare
Controversy for Mgmt
Pt. Reyes N.S.- Tomales Point
Wander, proved they had Johne’s disease
Mycobacterium leprae (& less commonly M. lepromatosis)
Leprosy (human disease)
Armadillo- only non primate to suffer from it
Leprosy
Armadillos can transmit it to humans
Esp in TX & LA
Humans probably gave it to armadillos 1st!
400-500 years ago
Leprosy in Humans (Hansen’s Disease)- the extremes
Tuberculoid leprosy- “Strong Immunity” non-pruritic rash (rash that doesn’t itch), mild peripheral nerve damage (numbness). Few bacteria (grow to have strong immunity)
Lepromatous leprosy: “Weak Immunity” skin nodules or plaques loaded with M. leprae. May have severe peripheral nerve damage. May lose eyelashes & eyebrows, body hair, nails, ulcers (may get infected and → death)
Dx: Skin biopsy- look for disseminated lesions with acid fast bacteria
Do Hansen’s Patients’ limbs fall off?
NO
Leprosy in Armadillos
Why? Relatively low body temp & “Weak” immune response
For every 5 exposed/infected only 1 has clinical disease
Lepromatous Disease most common (more severe, die)
Dx: Ear biopsy- dissemated disease w/ acid fast bacteria
M. Leprae
Does NOT live long in environment (2 weeks max under moist conditions)
Transmission route- close contact with an untreated person (or Armadillo) who has it (respiratory?)
Handling Armadillos not advised- especially if they appear sick!
Questions
Do any Mycobacteria spp have significant population level impacts on wildlife? No, can transmit to LS and be shared with humans)
Why are they important?