Avian Bacteriology Flashcards
What are the typicla Mycobacterium species that affect avian species?
How prevalent is this disease?
What are the most commonly affected species?
Is there a demographic group that is overrepresented?
Etiology and prevalence of Avian Mycobacteriosis
- Described in companion, zoo, and free-ranging birds
- Caused by tuberculous and atypical nontuberculous species
- Most are nontuberculous and involve species such as M genavense and M avium
- Tuberculous species rarely reported in birds
- One survey of pet psittacine suggested in infection rate of 0.5-14%
- Most commonly affected psittacines: brotogerid parakeets, amazons, buudgies, and pionus parrots
- Slow growing organism, tends to be a disease of older birds
How are birds exposed to mycobacteria?
Is this disease contagious?
What organ systems are typically affected?
How do the lesions between tuberculous and nontuberulous mycobacteria differ?
Exposure
- Nontuberculous species commonly found in the environment
- Infection through ingestion of water or contact with infected soil
- No confirmed cases of bird to bird transmission, however outbreaks have occurred in free-ranging non-psittacine birds, though this could be due to poor conditions and immunosuppression
- Uncertain if immunocompromise is required for disease in individual captive birds
- Sporadic cases of M tuberculosis have been reported in birds
- Can infect GI, liver, resp, bone, dermis, and other organ systems
- Ingestion—small intestines and liver—hematogenous spread
- Inhalation may lead to pulmonary infections
- Nontuberculous species tend to cause diffuse enlargement of the affected organ, often without visible granulomas. In contrast M tuberculosis tends to produce visible nodules
What are the clinical signs typically associated with avian mycobacteriosis?
What clinicopathologic changes are typically associated with infection?
What changes on imaging may be seen?
How is this disease diagnosed?
Clinical presentation
- Generally nonspecific clinical signs
- Weight loss, pu/pd, poor feathering, diarrhea, coelomic distension, resp signs
- Can have facial/oral lesions
- Lab findings typically nonspecific, however can see moderate leukocytosis characterized by heterophilia and monocytosis, sometimes anemia of chronic disease
- If liver is infected can see increases in AST, ALT, LDH, BA
- Rads can show enlarged liver and spleen, thickened GI, and pulmonary lesions
- Diagnosis of cutaneous lesions through biopsy, cytology, histopath etc
- Diagnosis of internal disease more difficult, often diagnosed post mortem
- PCR of feces and target tissues can be helpful
- Intradermal testing correlates poorly with presence of disease in birds
- Culture of fecals is possible but difficult, may take 1-6 months to grow
Is avian mycobacteria zoonotic?
How should such cases be handled?
Zoonotic considerations
- Human infection with M tuberculosis is of serious concern, euthanasia often recommended for any birds found to be positive
- Atypical mycobacteriosis is extremely rare in immunocompetent humans
- M avium very common in AIDS patients (up to 40% if no preventive treatment)
- These infections are likely from the environment, but caution should still be used
How is avian mycobacteriosis treated?
How successful is treatment?
How long is treatment recommended typically?
Treatment
- Both successes and failures have been reported
- Treatment should be considered on a case by case basis
- No one specific combination that is proven effective, recommendations based off of human literature
- Enrofloxacin, rifampin, ethambutol and clarithromycin are common, usually di or tritherapy
- Judging response to therapy can also be challenging, especially if diagnosis was based on biopsy of an organ.
- Shedding will remain intermittent so repeated PCR unlikely to be of great benefit
- Treatment for a year or longer typically recommended
Psittacosis is caused by what etiologic agent?
What type of bacteria is this?
Describe the replication cycle of this bacteria.
How does it inhibit cellular defense mechanisms?
Chlamydiosis (Psittacosis)
- Definition
- Infectious, contagious disease caused by intracellular, gram-negative Chlamydia psittaci
- Historical data
- Named Psittacosis in 1940s
- Etiology
- Reclassified as Chlamydophila psittaci in late 1990s, merged with Chlamydia in 2009
- 9 species in genus Chlamydia
- Gram-negative bacterium, intracellular obligate parasite, has specific energy needs and cannot move
- Replication cycle
- Attachment and penetration of target cell by cytotoxic elementary bodies
- Enveloped into vesicle that fuses with lysosomes, then transforms into reticulated body
- ATP transferred into vesicle with help of ATP-ADPO translocase, produced by C. psittaci
-
C. psittaci has nearly complete peptidoglycan synthesis pathway
- Can also produce its own ATP
- Proteases lyse host cell and EBs are released – 48-hour cycle
- Host cell permanently infected and can infect macrophages and their progeny
- Under stress, RBs turn into ABs (aberrant bodies) which persist inside host cells
- Conclusions
-
C. psittaci can inhibit cellular defense mechanisms
- Inhibition of phagolysosomes in macrophages compromises immune response
- High variability in C. psittaci is determined by MOMP
- Persistence of C. psittaci in macrophages naturally selects strain with low virulence for that species (maybe high in other species)
- Persistent infections have been associated with a range of chronic infections
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C. psittaci can inhibit cellular defense mechanisms
How is avian chlamydia transmitted?
Describe the timeline from infection to clinical signs.
How can chlamydia be disinfected from the environment?
What makes Chlamydia pathogenic?
What are the clinical signs associated with Avian Chlamydiosis?
What are the case definitions for a confirmed, probable, or suspected case?
- Transmission
- EBs can be found in feces, urine, tears, nasal discharge, oropharyngeal mucus, and crop milk
- Infection occurs by inhalation or ingestion of infectious particles
- Infection is rapid and C. psittaci will replicate in lungs, air sacs, pericardium 24 hours after infection
- Within 48 hours, in bloodstream
- Within 72 hours, bird can shed into environment
- Vertical transmission demonstrated in duck, black-headed gull, and budgies
- Direct transmission from dogs, cats, horses, pigs, humans to conspecifics does not occur
- Resistance of C. psittaci
- EBs can survive outside/inside host cells for several weeks
- Free EBs in environment sensitive to heat and inactivated by formaldehyde 1% (not quat, lipid solvents)
- Hydrogen peroxide may have some efficacy
- Benzalkonium chloride can eliminate infectivity
- Pathogenicity
- Toxin is most important virulence factor, which is bound to EBs
- Clinical infection depends on relationship between EBs and macrophages
- Clinical features
- Acute, subacute, chronic forms described
- Respiratory signs, dyspnea, oculonasal discharge, anorexia, regurgitation, vomiting, green diarrhea
- Avian chlamydiosis
- Clinical signs: lethargy, anorexia, ruffled feathers, oculonasal discharge, conjunctivitis, diarrhea, green urates
- Case definitions in birds
- Confirmed case: isolation of C. psittaci from specimen, antigen in tissues by IFA, >4x titer increase, ID of chlamydiaceae in macrophages on microscopy
- Probable case: single high titer, antigen/PCR/antibody in feces, cloacal swab, respiratory/ocular exudate
- Suspected case: compatible illness, high titer but no signs/antigen, clinical signs with positive results from non-standard test, compatible illness that responds to therapy
How does psittacosis present in people?
- Psittacosis in humans
- 5-14 day incubation
- Fever, chills, headache, muscle ache, dry cough, upper respiratory signs
- Published case definitions available, similar to above
How is Avian Chlamydiosis diagnosed?
What is the preferred test?
What clinical findings are suggestive of this disease?
- Diagnosis
- Clinical diagnosis
- Anemia (<30%), marked leukocytosis (>30,000), heterophilia (>70-80%)
- Increased AST, LDH, CPK, bile acids
- Pneumonia, airsacculitis, splenomegaly on imaging/endoscopy
- Isolation of C. psittaci
- Aseptic collection of samples from throat/choana, but fecal, cloacal, conjunctival swabs can also be used (also peritoneal or air sac exudate)
- Collect for 3-5 consecutive days
- Isolation of chlamydiae in eukaryotic cell cultures
- Cell cultures one of the best methods for isolation, but is costly
- Cell cultures checked on day 2-3 and 5-6
- Direct immunofluorescence preferred
- Isolation on embryonated eggs
- Inject inoculum into yolk sac of 6-7 day embryos and incubate
- Causes death in 3-10 days
- If no death, vascular congestion collected and tested
- Histochemical stains
- Giemsa, Gimenez, Ziehl-Neelsen, and Macchiavello stains are normally used
- Immunohistochemical staining
- Monoclonal and polyclonal antibodies have been used
- ELISA
- Cross-reactions may lead to false positive results
- Reduced false positives in new kits fir monoclonal Abs, though sensitivity is reduced
- PCR
- Preferred as rapid, reliable, sensitive and can be used on nonviable specimens
- Serology tests
- Complement fixation test
- Sensitivity significantly less than 100%, though eats of collection make it ideal for screening large numbers of samples
- Other tests
- ELISA, latex agglutination, EB agglutination, microimmunofluorescence, agar gel immunodiffusion
- Complement fixation test
- Clinical diagnosis
What is the treatment for Chlamydia psittaci?
- Therapy
- Traditional treatment is tetracyclines for 45 days
- Doxycycline is first choice
- IM protocol with intermittent administration
- 400-600mg per liter of water based on species
- Medicated food (with chlortetracycline) can give good results
- Direct oral treatment practical (25-50mg/kg PO Q24 based on species)
- Fluoroquinolones or macrolides have been proposed
What is the etiologic agent of Fowl Cholera?
What species are particularly affected? What species are potential carriers?
Where is this disease found geographically?
What is the morbidity and mortality like?
Is it seasonal?
What are the typical clinical signs?
How is it transmitted?
What are the typical lesions?
How is it diagnosed?
How is it controlled?
Are people affected?
Avian cholera
- Pasteurella multocida: 16 serotypes
- Fowl cholera, avian pasteurellosis, avian hemorrhagic septicemia
- Multiple: esp waterfowl, coots. Less: crows, gulls. Mammals susceptible too, mice and rabbits high mortality. Some pig strains highly virulent to poultry.
- No. America. Specifically: 1) Central valley California 2) No. Calif and Oregon 3) Texas Panhandle 4) Nebraska waterbasin (south-central)
- Mortality can be high e.g. 50%, even 80% in areas of high population density
- Year-round, prevalent late summer, fall, winter. Follows flyways
- Acute, large die-off. Lethargic, drowsy. Die shortly after handling. Convulsions. Similar to duck plague and lead poisoning. Sudden death. Good body cond.
- Aerosol, oral (secretions not feces), vector, direct: mucous membranes of pharynx (URT). Abrasions in skin, conjuctiva. Carrier birds; hot spots in U.S.
- Good adipose, food in GI. Heart liver and gizzard hemorrhage. LITTLE white to yellow spots on the liver. Chronic: copper tone to liver. Paintbrush lesions.
- Culture: heart blood, liver, bone marrow (persists weeks to months in bone marrow). Smear blood and look for safety pin shaped organisms. Serology.
- Early detection. Immediate carcass removal. Gulls and crows transmit cholera because they aren’t as susceptible-decrease pops. Habitat management.
- Vaccination with bacterins successful; post exposure treatment w/oxytet. Production facilities.
- Snow geese are carriers. Found for several weeks in water (e.g. wetlands); 4 mo in soil.
- Possible-but unlikely. Humans usually get it from bites or scratches. Possibly aerosol.
What are the mycoplasma species that commonly affect birds?
What birds are particularly susceptible? Which mycoplasma are they susceptible to?
What is the geography of this disease?
What is the morbidity and mortality like?
Is there a seasonality to mycoplasmosis?
What are the typicla lesions and clinical signs?
How is this disease controlled?
Mycoplasmosis
- Mycoplasma gallisepticum (MG), M. meleagridis (MM), and M. synoviae (MS)
- Chronic respiratory disease, infectious sinusitis, house finch conjuctivitis
- House finch, goldfinch, ducks, geese. Falcons, Amazon parrot. MM=turkeys. MS=natural hosts chicken, turkey, guinea fowl.
- Worldwide.
- High morb low mort ducklings Mort 7-30% goslings. Morb 15-25%, mortality 3-8% in 3-4 week old goslings
- None really. Colder weather encourages birds to eat at feeders more.
- Poultry signs more severe than house finch. Puffy swollen eyes, crusty eyelids, Foamy eyes, excessive tearing. URT (severe infection).
- Direct. Feco-oral. Aerosol. Vertical (eggs)
- Mild to severe inflammation of the eyes, discharge from nares.
- Giemsa-stained impression smears: intracytoplasmic inclusion bodies, culture and isolation of the organism
- Routine cleaning of bird feeders; Bleach.
- None reported
- Lack cell walls, possess plasma membranes. Fastidious, difficult to grow, have intimate dependence on the host species which they colonize and grow slowly on artificial media.
What is the etiologic agent of New Duck Disease, aka Fibrinous Serositis?
What species are commonly affected?
Where is this disease located?
What is the morbidity and mortality like?
What are the typical lesions and clinical signs?
When are birds affected?
New Duck Disease
- Reimerilla anatipestifer aka Fibrinous Serositis
- Black swans, snow geese. Turkeys, chickens, pheasant, quail, waterfowl
- Tasmania, Canada
- Young mortalities
- Listless, droopy. Fluid d/c from eyes, nares. Green diarrhea, neurology.
- Fibrinous covering on organs
- Death 24-48hr after incubation.
What is the etiologic agent of necrotic (hemorrhagic) enteritis?
What birds are particularly susceptible?
What is mortality like?
Is there a seaonsality to this disease?
How is it transmitted?
What are the typical clinical signs and lesions?
How is it diagnosed?
Necrotic enteritis
- Clostridium perfringens type C
- Haemorrhagic enteritis; Clostridial enteritis; Rot gut
- Mallard, black ducks, Geese
- Worldwide.
- Variable mortality: from less than 1% to 40%
- Fall/winter
- Depression, inappetance and sudden death; necrotic and/or haemorrhagic enteritis.
- Feco-oral
- Necrotic enteritis, esp ileum. Serosanguinous fluid or blood in lumen (early in disease), fibrino-necrotic membrane. Foul smell. Whole grains present.
- Lg # gram-positive bacteria; Isolation and ID of Clostridium perfringens. Testing for toxigenic status of Clostridium perfringens
What is the etiologic agent of ulcerative enteritis - aka quail disease?
What species are commonly affected?
What is the morbidity and mortality like?
What are the typical clinical signs and lesions?
Ulcerative enteritis
- Clostridium colinum
- Quail disease
- Quail, outbreaks rare. Pheasant. Partridge. Grouse.
- Mort 100%
- Sudden onset, rapid spread.
- Ulcers in intestine, hemorrhagic rings. Liver: necrotic areas=yellow spots.
