cientific principles of bacteriology are uni-versal; however, in application, bacteria canadapt to their avian hosts, altering the formand pathogenicity of well known bacterial

species. Avian bacteriology is further complicated bythe fact that bacteria that are as yet taxonomicallyundescribed can be isolated from a variety of avianspecies. Some of these bacterial strains have beenerroneously classified as taxons (eg, Pasteurellahaemolytica, Alcaligenes faecalis). In general, bacte-rial adaption to an avian host minimizes cross-spe-cies transmission from birds to mammals. Non-host-adapted transmission usually requires largenumbers of organisms, repeated exposures, specificsusceptibility or immunosuppression. Some host-adapted strains may form biovars that are specific toone avian species (or a few closely related species) ascompared to the dominant species.

Example of Bacterial Taxonomy:Genus SalmonellaSpecies S. typhimuriumSubspecies S. typhimurium var copenhagenBiovar Pigeon strains, chicken strains

Bacterial infections may be primary or secondary.This differentiation is important for the evaluation ofa disease process. After becoming established, manysecondary invaders are able to maintain a diseaseprocess independent of other infectious agents orpredisposing conditions. Laboratory examinations(biochemical or serologic) are rarely of any help indifferentiating primary from secondary invaders.The companion bird clinician must determine theimportance of bacterial isolation for a specific birdspecies and a specific disease process. Analogous con-clusions drawn from poultry literature may not bevalid, and experimental infections are frequently notpossible. Some specific points may guide the clinicianin interpreting bacterial culture results (Table 33.1).

S C H A P T E R

33BACTERIA

Helga Gerlach

Because the isolation of “unusual” bacteria can beexpected from avian samples, the clinician can en-hance results by providing the laboratory with athorough anamnesis, exact species of the bird inquestion, and as far as possible, the names of particu-lar bacteria that may be suspected in the case. Thislatter point is especially important if special mediaor environmental conditions are needed for bacterialisolation. In addition, with some organisms, specialtransport media and shipping methods (eg, on ice)may be necessary to preserve the organism.

Blood cultures are considered a definitive diagnostictool in humans and some mammals. In these species,samples are, as a rule, taken during a period of fever.A febrile period is difficult to determine in a bird andis generally considered of minimal importance. Inbirds, organs as well as blood are not necessarilysterile, although the number of bacteria is extremelylow. Generally, the isolation of small quantities of

autochthonous flora is considered normal, and onlythe isolation of primary pathogens is really helpful.Because whole blood has bacteriostatic and bacteri-cidal properties, blood culture samples must betransferred immediately after collection to attenuantcontaining nutrients and one of the artificial hepari-noids, for instance Na-polyanetholsulfate. Commer-cially available blood culture flasks are also useful.

Gram-negative Bacteriaof Clinical Significance

“Intestinal bacteria” are considered to be those spe-cies that can colonize the intestinal tract. As a group,intestinal bacteria can be part of the normal flora orpathogenic organisms that are not routinely found inthe GI tract; in some cases, normal flora can becomesecondary pathogens. When a bacterium leaves themucosal surface and penetrates the intestinal wall,it then can induce systemic disease, including septi-cemia and death. The Enterobacteriaceae are consid-ered the most important avian intestinal pathogens,but other groups, such as Aeromonas, Pseudomonas,Alcaligenes, Bordetella spp. and related organisms,as well as Vibrio and Campylobacter, may also colo-nize the gastrointestinal tract.

Enterobacteriaceae

The members of the Enterobacteriaceae family typi-cally grow well on commonly used media. Enterobac-teriaceae are divided into genera based on specificbiochemical and serologic characteristics. Many spe-cies are further divided into biotypes and serotypes.In these species, complete identification requires dif-ferentiation between the O, K and (in motile species)H antigens. Serologic differentiation between thegenera is often difficult since group-specific antigens(lipopolysaccharides) can cross-react.

Enterobacteriaceae are able to propagate in the envi-ronment if they are in the proper conditions. Entero-bacteriaceae are ubiquitous and considered to be partof the autochthonous intestinal flora in many mam-mals, including humans and some species of birds(Table 33.2).

TABLE 33.1 Guides to Interpretation of Bacterial Culture Results27

Isolation of an organism in an almost pure culture (approxi-mately 80% of the colonies present) may indicate that thebacteria is a component in the disease process.

Isolating large numbers of bacteria in almost pure culture fromthe heart tissue is suggestive of bacteremia, and the isolatedagent should be considered part of the disease process.

Isolating a bacteria that is part of the autochthonous flora mayindicate that it is functioning as an opportunistic (secondary)pathogen.

If the isolated organism has pathogenicity markers, it is prob-ably involved in the disease process. It is not possible todetermine if the bacteria is a primary or secondary pathogen.

Isolating bacteria from parenchyma with pathologic or his-topathologic lesions suggests that the agent contributed to thedisease process.

Isolating a bacterium without identifying other microorganisms(virus, chlamydia, other bacteria, fungi, protozoa) suggests thatthe agent is a primary pathogen. Finding virus or chlamydiasuggests that the bacterium may be a secondary pathogen.Isolation of bacteria from a bird with fungi and protozoa sug-gests that the bacterium is a primary pathogen.

Obtaining mixed cultures or identifying individuals within agiven flock with different bacterial isolates suggests secondaryinfections are occurring.

Isolating small to moderate numbers of bacteria from the liveror kidney can be “normal,” because birds have hepatic andrenal portal circulations and lack lymph nodes that filter bloodbefore it drains into the liver and kidney. Because lymph folliclesare distributed throughout these organs, defense responsesactually occur within the parenchyma and not externally, as inmammals. These organs should not be expected to be sterile,but should be expected to contain autochthonous flora. Thenumber of organisms isolated at necropsy depends on the timeof death and the method of handling the body (eg, storage,preservation).

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Isolation of Enterobacteriaceae from the respiratoryor reproductive tracts is abnormal. This group ofbacteria can colonize most avian tissues, where it isfrequently considered as a secondary pathogen. Insome cases, Enterobacteriaceae can function as pri-mary pathogens. Substantial differences exist in thevirulence of the various Enterobacteriaceae and inthe host response to infections. The genera Shigellaand Edwardsiella are normally not cultured frombirds (the latter rarely from pigeons). The generaEnterobacter, Hafnia, Serratia and Proteus are of alow pathogenicity. The isolation of Enterobacter ag-glomerans (a plant pathogen) in avian feces can indi-cate the consumption of seeds that contain more than106 bacteria/g of food. This bacterium is common indecaying plant matter; foods containing the bacte-rium in high numbers should be considered toxic.Serratia marcescens is increasingly found in largeparrots with chronic debilitating diseases. Predispos-ing factors seem to include previous antibiotic treat-ment and immunosuppression.

Escherichia (E.)

E. coli is the most commonly encountered member ofthis genus; in many avian species it is considered tobe a more important pathogen than salmonella (seeTable 33.6). This genus contains a number of speciesthat may be motile or nonmotile, encapsulated ornonencapsulated. Classification of the strains of E.coli that infect birds has been difficult. The serologicand virulence factors used to classify the E. colistrains that infect humans and other mammals donot accurately predict which E. coli strains will bepathogenic in birds. Although each serovar of E. coliincludes both virulent and avirulent strains, thereseems to be a slightly higher frequency of virulentstrains within the serovars 01, 02 and 078. In experi-mental transmission studies, all lysine decarboxy-lase-negative E. coli strains have been found to bevirulent in birds. Unfortunately, many of the lysinedecarboxylase-positive strains are also virulent.

Pathogenesis The pathogenesis of E. coli infections in birds ispoorly defined. Mammalian strains produce largequantities of exotoxins that cause many of the clini-cal and pathologic changes associated with infection.Except for the presence of enterotoxins, avian E. colistrains appear to produce few exotoxins. These en-terotoxins cause diarrhea by inducing hypersecretionof fluids into the intestinal lumen. Endotoxins maycause hypersensitivity angiitis followed by septice-mia and death.

Clinical Disease and PathologyThe clinical signs associated with primary or secon-dary infections are thought to be governed by theportal of entry to the avian host.

Colisepticemia is characterized by an acute onset oflethargy, anorexia, ruffled plumage, diarrhea andpolyuria. E. coli septicemia usually involves the kid-neys, although clinical signs of renal involvementmay or may not be present. CNS involvement is rare.Ocular lesions occasionally occur and include exuda-tion of fibrin into the anterior eye chamber or uveitis.Serofibrinous arthritis can occur as a sequela in someinfected birds. Fibrinous polyserositis, the severity ofwhich depends on the chronicity of the infection, maybe noted at necropsy. Catarrhal enteritis is commonbut nonspecific. The most consistent histologic lesionis serofibrinous inflammation with plasma cell infil-tration in the liver and kidneys (Figure 33.1).

Localized enteritis caused by E. coli is a result ofenterotoxin production, which induces an increasedsecretion of fluids. The resulting diarrhea causes asubstantial loss of electrolytes and proteins and in-duces dehydration and cachexia. Some strains of E.coli are capable of colonizing and destroying the in-testinal epithelium. These strains typically induce apseudomembranous or ulcerative enteritis. Clini-cally infected birds die peracutely or develop nonspe-cific signs associated with enteritis. Infections withthese strains are usually diagnosed on postmortemexamination.

Coligranulomatosis (Hjaerre’s disease) is particu-larly common in Phasianiformes including chickens,turkeys, peafowl, partridges and capercaillie. Mucoid(eg, encapsulated) E. coli strains, mainly of serovars08, 09 and 016, are the usual etiologic agents. Coli-granulomas are thought to occur when other agentsdamage the intestinal mucosa and allow a secondaryinfection with specific E. coli serovars. It is currently

TABLE 33.2 Birds in which Enterobacteriaceae are not normal

Psittaciformes (parrots andparakeets)

Fringillidae (finches)

Ploceidae (weaver finches)

Astrildae (waxbills)

Accipitriformes (hawks,vultures)

Falconiformes (falcons)

Strigiformes (owls)

Gruiformes (cranes)

Otididae (bustards)

Sphenisciformes (penguins)

Ciconiiformes (storks, ibises)

Tetraoninae (grouse)

Musophagiformes (turacos)

Trochiliformes (humming-birds)

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thought that galactans found in the E. coli capsulestimulate the granulomatous reaction.

Affected birds develop diarrhea, polyuria and chronicweight loss. Granulomatous dermatitis is occasion-ally noted. Grayish foci of varying sizes in the liver,intestinal subserosa and spleen or kidney are typicalfindings at necropsy. These granulomas are distinctfrom those induced by avian tuberculosis becausethey lack an opening into the intestinal lumen. Thecenter of the foci may be mineralized. Histologicchanges are characterized by multinucleated giantcells and a few heterophils around a central necroticregion. Acid-fast staining should be used to rule outmycobacteriosis.

E. coli can cause a primary rhinitis but is generally asequela to infections elsewhere in the body. Air saclesions can be severe and may extend to the perito-neum, causing a fibrinous polyserositis. Except for ingeese, E. coli pneumonia is rare. This is due to thespecial anatomy of the avian lung. When pneumoniaoccurs, it is most common in young chicks that haveinhaled a high number of virulent E. coli with con-taminated dust. Affected birds are usually dyspneicand cyanotic. In contrast to mammals, pneumonia isnot associated with prominent respiratory sounds.

Hens can develop E. coli infections characterized byfibrinous salpingitis or oophoritis originating fromorganisms that ascend from the cloaca or by imprint

metastases from infected air sacs. Infections are usu-ally chronic in nature, with untreated birds eventu-ally dying from salpingoperitonitis. Genital tract in-fections in males are less common, but when they dooccur they usually result in orchitis and permanentsterility.

Secondary colonization of joints and bone marrowcan occur following E. coli septicemia. These lesionsare rare, but when the do occur they are most fre-quent in nestlings and fledglings. Some of the finchspecies seem to be particularly susceptible. Bonemarrow infections appear to be very painful, andaffected birds are usually reluctant to move.

DiagnosisPolyserositis and granuloma formation are lesionssuggestive of E. coli infections. Specific diagnosisrequires culturing the organism from infected tis-sues. Serotyping is of academic importance.

TreatmentThe ability of a selected drug to penetrate targettissues or granulomas must be considered (see Table33.7). Oral antibiotics may be effective in treating E.coli infections limited to the intestinal mucosa, butparenteral antibiotics are necessary for treating mostE. coli infections. In addition to antibiotics, therapeu-tic considerations should also include administrationof avian lactobacilli in an effort to lower the intestinal

FIG 33.1 A seven-year-old male Amazon parrot was presented for weakness and diarrhea. Abnormal clinical pathology findings includedPCV=22, WBC=33,000, SGOT=476. A Gram’s stain of the excrement revealed 70% gram-negative rods. Radiographs indicated ileus (gaseousdistension of the bowel), a full crop and microhepatia. Dried excrement is visible pericloacally. The dilated bowel loops are displacing theproventriculus (p) cranially and the ventriculus (v), liver (l) and heart (h) ventrally.

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tract pH and help establish a proper autochthonousflora. Mammalian strains of lactobacillus can be ef-fective in changing the intestinal pH but require theadministration of large quantities of product over athree- to four-week period. Lactulose may also behelpful in lowering the intestinal pH. Providing anutritional diet is important in improving gastroin-testinal physiology in malnourished birds.

Salmonella (S.)

The genus Salmonella includes approximately 2000species divided into five subgenera. Subgenus I is themost important in birds. Subgenus III (S. arizonae,Arizona hinshawii) has occasionallybeen reported in birds, particularlythose that are in contact with rep-tiles. Most strains are motile andgrow on common media. The subgen-era are determined by specific bio-chemical profiles, and species are dif-ferentiated serologically (O, K [Vi]and H antigens). Lysotyping is usedfor further characterization at the re-search level. Propagation can occuroutside the host if the correct ambi-ent temperatures and proper nutri-ents are available.

Most vertebrates can be infectedwith some Salmonella spp. However,the host susceptibility and develop-ment of carrier states vary widelyamong species. Free-ranging birdscan be subclinical carriers and serveas a reservoir for the aviary. In addi-tion to free-ranging birds, rats, fliesand other vermin may also serve asvectors of salmonella. Avian specieswithout ceca or with involuted cecaappear to be more susceptible to sal-monella infections than birds withfully functioning ceca. Bacteroidesand Spherophorus spp. are consid-ered autochthonous cecal flora, andthese gram-negative anaerobes mayfunction as natural antagonists forSalmonella spp. The incidence ofvarious S. spp. seems to vary withgeographic location and the types offood consumed, particularly the pro-teinaceous component. Importedbirds (and other animals) may serveas reservoirs for nonindigenous S.

spp. that can cause devastating outbreaks. Somesalmonella strains are host-adapted (eg, S. galli-narum-pullorum to chickens, S. typhimurium var.copenhagen [in two biovars] to either pigeons [malon-ate-negative] or European finches [malonate-positive]).

TransmissionSalmonella enters the host principally through theoral route. Contaminated dust from feces or feathersmay be involved in aerogenic spread in some cases.Egg transmission can occur with fully walled andL-form salmonella. It is most common with adaptedstrains but is possible with any S. sp. Experimentalstudies indicate that patent infections in embryosoccur with fewer than ten bacteria. These infected

FIG 33.2 An adult Barn Owl from a zoological collection had a three-year history ofintermittent depression and anorexia. The bird was presented with severe right-sidedhead tilt and vertical-to-rotatory nystagmus. The external ear canal was hyperemic, andthe tympanic membrane was opaque and edematous. Radiographs indicated a soft tissuedensity in the right tympanic bullae suggesting an internal ear infection. Auditory evokepotentials indicated lesions in the peripheral and central auditory pathways. Klebsiellasp. and Pseudomonas sp. were recovered from the infratrochlear area and brainstem atnecropsy.

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chicks then hatch and spread salmonella by directcontact throughout a nursery. If an embryo has morethan ten bacteria, it usually dies before hatching.47 Infreshly hatched chicks, salmonella often serves asthe first bacterium to colonize the intestines. Thisorganism becomes host-adapted during the egg incu-bation period, and the hatched chick can then serveas a subclinical carrier. In some cases, the salmonellainfection can eventually induce a septicemia anddeath. Subclinical carriers allow an infective cycle tooccur in the absence of other vectors. Vertical infec-tions may also occur if infected hens feed their youngcontaminated crop contents.

PathogenesisOne of the characteristics of the group Enterobacte-riaceae is that they all produce endotoxins. Salmo-

nella is no exception, and some cases of food poison-ing are linked to this bacterium. Indirect deaththrough endotoxin contamination of food is rare inbirds; most avian salmonella problems are associ-ated with direct infections. Interestingly, both viru-lent and nonvirulent strains of a given Salmonellasp. can exist simultaneously in a host. Virulentstrains are those that can penetrate an intact intes-tinal mucosa, and nonvirulent strains are those thatrequire a mucosal lesion to enter a host. Nonvirulentstrains often colonize the gut, resulting in asympto-matic infections and intermittent shedding. Oncevirulent or nonvirulent strains have passed the mu-cosal barriers, they induce a septicemia that resultsin an immune response or colonization in tissues andeventual death of the bird. In some cases, Salmonellasp. may cause chronic infections that are charac-terized by intermittent septicemia and clinical signs.Recurrent infections usually result in progressiveorgan involvement; the CNS and joints are fre-quently end-stage sites of infection.

IncubationIncubation periods vary with the type of salmonellainfection. Presumably, these differences are depend-ent on the strain of infecting salmonella, the route ofinfection and the condition of the host. In acute dis-eases, incubation periods are typically three to fivedays. With egg transmission the incubation period isshorter, generally considered to be two days. Sub-clinical carriers can have prolonged incubation peri-ods.

Clinical Disease and PathologyAcute diseases are characterized by nonspecific signsincluding lethargy, anorexia, polydipsia (sometimesfollowed by polyuria) and diarrhea. In subacute tochronic cases, CNS signs, arthritis (particularly inpigeons), dyspnea and indications of liver, spleen,kidney or heart damage are common. With high-doseinfections, conjunctivitis, iridocyclitis and pano-phthalmia may occur.

Some individual avian species have unique clinicalpresentations. Outbreaks in lories (Loriidae) andpenguins (particularly Jackass Penguins) are associ-ated with peracute diseases and high flock mortality.African Grey Parrots are also very susceptible, buttypically develop a more chronic disease exhibitingphlegmon, granulomatous dermatitis, arthritis andtenovaginitis (Figure 33.3). Respiratory signs withmyocardial lesions are common in tangares,quetzals, Red-headed Barbets, terns and HouseSparrows. Nonspecific CNS signs are common in

TABLE 33.3 Percentage of Psittaciformes Shedding Gram-negative Bacteria and Yeast

Bare-eyed Cockatoo 44 0 0 13 6

Citron-crested Cockatoo 30 0 0 0 0

Major Mitchell’s Cockatoo 27 20 0 0 13

Moluccan Cockatoo 81 13 0 0 13

Sulphur-crested Cockatoo 44 0 0 0 11

Triton Cockatoo 84 8 3 0 0

Red-vented Cockatoo 78 0 0 0 0

Umbrella Cockatoo 56 24 4 0 15

Rose-breasted Cockatoo 16 2 0 0 0

African Grey Parrot 17 0 0 0 0

Eclectus Parrot 10 0 0 0 10

Blue-crowned Amazon Parrot 0 0 0 0 0

Blue-fronted Amazon Parrot 20 0 0 0 0

Yellow-headed Amazon Parrot 12 0 0 0 0

Yellow-naped Amazon Parrot 38 0 0 0 6

Blue and Gold Macaw 23 0 0 8 8

Buffon’s Macaw 23 0 0 8 8

Green-winged Macaw 26 3 0 3 3

Military Macaw 20 4 0 0 16

Red-fronted Macaw 7 7 0 0 0

Scarlet Macaw 19 2 0 0 0

Hyacinth Macaw 6 0 0 0 11

Incidence (in percent) of the isolation of gram-negative bacteria and yeast fromthe cloaca of a group of psittacine birds with no observed clinical abnormalities.Gram-positive bacteria were isolated from 91% of the 506 cloacal samples. It isnot unusual to find transient populations of gram-negative bacteria in the cloacaof asymptomatic birds. However, the presence of these bacteria in the gastro-intestinal tract can cause problems if a bird is stressed. The isolation ofgram-negative bacteria from clinically asymptomatic psittacine birds warrants aclose examination of management practices. Adapted from Flammer K: AvianDis 32: 79-83, 1988.

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Ent

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Kle

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Pseu

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SECTION FIVE DISEASE ETIOLOGIES

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geese and ducks. Some infectedducks will swim with an invertedkeel (keel disease) just prior to death.Subacute salmonellosis in manyfinches (Fringillidae) is charac-terized by granulomatous ingluvitisthat may be confused with candidainfections. Granulomatous dermati-tis has been reported in several spe-cies and is thought to be induced bymosquitoes or other biting insects.

Subgenus III strains are consideredless virulent than those of subgenusI; however, the clinical lesions in-duced by this subgenus are indistin-guishable. Ocular lesions appear tobe more frequent with subgenus III,and turkeys, ducks, parrots and ca-naries are particularly susceptible.

Postmortem lesions include dehydra-tion, degeneration or necrosis ofskeletal musculature, gastroenteri-tis (occasionally with ulcers andgranulomas), enlargement of theliver and spleen (with or without dis-seminated small whitish foci), bilecongestion and nephropathy. Chronic infections usu-ally cause pericarditis or epicarditis fibrinosa, granu-loma formation in the liver, spleen and kidney, anddegeneration or inflammation of the ovary or testis.Fibrin filling the cecal lumen is a common finding.

Histopathologic changes are nonspecific with puru-lent inflammation in the parenchymal organs.Granulomas are common with chronic infections. Pu-rulent leptomeningitis and exudate formation in thesubarachnoidal spaces are usually noted in birdswith CNS signs.

DiagnosisA confirmed diagnosis requires isolation and identi-fication of the Salmonella species. Serologic evalu-ation of a flock can be used only if the precise speciesis known; however, chronically infected subclinicalbirds are frequently serologically negative. The sameis true for birds infected with L-forms. The develop-ment of a serologic response requires penetration ofthe intestinal mucosa, and most subclinical carriershave infections limited to the intestinal lumen.

TreatmentWhether or not to treat salmonella infections in com-panion birds is controversial. The author believesthat clinically affected birds and companion birdsthat are identified as carriers should be treated be-cause of public health hazards. Therapy should in-clude appropriate antibiotics (based on sensitivity)and lactobacillus products. In general, the frequentlyencountered salmonella strains are sensitive to com-monly available antibiotics, but some strains fromfree-ranging birds (particularly from seagulls) dem-onstrate varying degrees of antimicrobial resistance.CNS signs and chronic infections tend to be refrac-tory to therapy. Flock management of salmonellashould concentrate on preventing egg transmissionby identifying and removing subclinically infectedbreeders. Treating birds that have egg-derived infec-tions is extremely difficult. Host-adapted strains ofsalmonella seem to cycle in periods of approximatelythree-month intervals. Cycles of egg transmissioncan best be broken by collecting eggs for future breed-ing stock four weeks after treating the parent stock.Newly hatched chicks from these birds should becultured (fecal swabs) at hatching, and infected birdsshould be treated immediately.

FIG 33.3 A three-month-old pigeon was presented with depression, anorexia, diarrheaand reluctance to move. An open ulcer was present on the bird’s hock. Salmonella sp. wasisolated from the bird’s feces and the bird responded to treatment with antibiotics(courtesy of Louise Bauck).

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Treatment of L-forms can be attempted with clin-damycin (100 mg/kg body weight) or a combination oferythromycin and ampicillin (both components at thefull dose).

ControlProper hygiene is the best tool for preventing salmo-nella outbreaks. The effective control of flies, rodentsand other vermin is essential (Figure 33.4). Regularcleaning and disinfection of the aviary and nursery,along with proper storage of food, are all importantin preventing salmonellosis. Several Salmonella spp.vaccines have been evaluated experimentally, butnone have proven to be effective.

Companion bird strains of Salmonella are not consid-ered important human pathogens in healthy indi-viduals, but can cause problems in infants, geriatricpatients or those with immunosuppressive diseases.Humans carrying salmonellosis can infect their com-panion birds. Such human-to-animal interactionshave been shown to occur with African Grey Parrots,Amazon parrots, cockatoos and macaws.

Citrobacter (C.)

The three species of Citrobacter (C. freundii, C.amalonaticus and C. diversus) are less commonlyencountered than other members of the Enterobacte-riaceae. C. freundii appears to be the most patho-genic of the group. C. diversus is rare in birds. Whenusing serologic assays it is important to know that C.

freundii antibodies often cross-react with those to S.typhimurium.

Citrobacter spp. cause serious secondary infections inweaver finches and waxbills. A rapid bacteremia fol-lowed by acute death occurs when the organismpenetrates the intestinal mucosa. Ostriches, particu-larly chicks and young birds, also appear to be verysusceptible to Citrobacter spp. Infected birds of anyspecies may die without any clinical signs, or theycan exhibit a brief period of depression and diarrheaprior to death. Postmortem changes indicate septice-mia (petechiation of the heart, musculature and pa-renchyma). Surviving birds frequently become carri-ers. C. amalonaticus is frequently recovered from theintestinal tract of normal Psittaciformes. Intestinalinfections would indicate that a disturbance has oc-curred in the autochthonous flora. A definitive diag-nosis requires culturing the organism from affectedtissues. The rule-out list is the same as for Salmo-nella spp. Therapeutic decisions should be based onappropriate culture and sensitivity. Neomycin deliv-ered by gavage is often effective in clearing intestinalinfections. In flock outbreaks, the same drug admin-istered in the drinking water may be helpful in con-trolling infections.

There have been no reported cases of citrobacterinfections in humans derived from exposure to in-fected birds.

Klebsiella (K.)

K. pneumoniae and K. oxytoca are frequently recov-ered from birds in which they can function as pri-mary pathogens, particularly in weaver finches, orthey can be involved as opportunists in immunosup-pressed or stressed patients. These organisms arenonmotile Enterobacteriaceae, and most members ofthe genus are encapsulated. The mucoid capsule pro-vides them with substantial protection from environ-mental extremes and many disinfectants. Heat anddrying are the best methods of killing Klebsiella spp.

Specific information on the transmission, pathogene-sis and incubation period for Klebsiella spp. in birdsis not available. The Klebsiella capsule provides abarrier to protect the organism from cellular immu-nity. However, the capsule is also highly antigenicand stimulates a protective humoral immune re-sponse. Klebsiella spp. bacteremia usually results inthe colonization of the kidney, causing renal failure.In chronic infections, the lungs may also be involved.In many bird groups (eg, pigeons, weaver finches,

FIG 33.4 Aviary hygiene is important in preventing a bird’s expo-sure to many infectious agents including bacteria. Walk-in typeenclosures have several disadvantages when compared to drop-through type enclosures. The birds in walk-in enclosures can fly tothe floor where pathogens can accumulate in excrement and foodwaste. Birds are more likely to come in contact with discharge fromflies or rodents that have ready access to organic waste on the floorof the enclosure. Additionally, caretakers can act as mechanicalvectors for the transmission of pathogens as they walk from oneenclosure into the next.

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goldfinches and siskins, geese, birds of prey, Amazonsand African Grey Parrots), infections are not de-tected until late in the disease process when respira-tory signs occur. Encephalomyelitis is occasionallynoted in terminal cases. While systemic klebsiellainfections are most common, local infections involv-ing the sinuses, skin, oral cavity and crop may alsooccur, particularly in Psittaciformes. The diagnosis ismade by isolation and identification of the organism.The rule-out list is the same as with salmonella.

Yersinia (Y.)

The genus Yersinia currently consists of eleven spe-cies.1 Unlike other Enterobacteriaceae, which arestrictly rod-shaped, Yersinia spp. form ovoid-to-coc-coid rods that replicate in the environment at ex-tremely low temperatures (+4°C) if provided theproper sources of organic nitrogen. Because the or-ganism can grow effectively at low temperatures,infections are particularly common during the wintermonths.

Y. pseudotuberculosis appears to be the most impor-tant avian pathogen. Y. intermedia, Y. frederikseniiand Y. kristensenii are frequently isolated from vari-ous avian species, but their pathogenicity remainsundetermined.

When grown at 20-28°C, Y. pseudotuberculosis is mo-tile; when grown at higher temperatures it is nonmo-tile. Six serovars have been distinguished. Serovar 1is most frequently isolated from birds. Y. pseudotu-berculosis has been recovered in an L-form from free-ranging urban pigeons.

TransmissionY. pseudotuberculosis is thought to be indigenous tonorthern and middle Europe. The occurrence of thisbacterium in other parts of the world including Can-ada, the United States, Africa and Australia isthought to have arisen from the movement of Euro-pean birds and rodents to other suitable geographiclocations. An unknown percentage of the free-rang-ing birds in Europe are considered asymptomaticcarriers.

Y. pseudotuberculosis infects a wide range of hosts,including many bird species and various mammals,particularly rodents and including humans. Toucans,toucanets, aracaris, barbets and turacos appear to beextremely susceptible.

Clinical Disease and PathologyY. pseudotuberculosis may be associated with per-acute, acute or chronic clinical disease. Peracutedeath without clinical signs is common in infectedPiciformes and Musophagidae. Clinical signs associ-ated with acute disease include lethargy, dehydra-tion, diarrhea and dyspnea. Emaciation, wasting andflaccid paresis or paralysis are common with sub-acute or chronic cases. Birds with a wasting syn-drome appear similar to animals infected with tuber-culosis. Infected ducks frequently develop tarsal jointswelling. Canaries may be severely dyspneic prior todeath.

Gross changes associated with peracute infectionsinclude swelling of the liver and spleen and bloody-to-fibrinous exudate into the body cavity. Submiliary-to-miliary, sharply demarcated grayish foci withinthe liver, lungs, spleen and kidneys are common withthe acute course. Chronic infections are charac-terized by granuloma formation in organs and theskeletal musculature. Ascites and osteomyelitis mayor may not be present. Ulcers in the proventriculus,ventriculus and duodenum may occur in infectedcanaries. Tarsitis chronica deformans with caseousexudate in the joint cavity is frequently seen inducks.

Coagulation necrosis and thrombophlebitis are thecommon histologic changes. In acute and chroniccases, inflammatory cells infiltrate the necrotic areasand eventually induce granulomas.

DiagnosisThe histopathologic changes, along with the identifi-cation of gram-negative coccoid rods, are suggestiveof Y. spp. infections. Definitive diagnosis requiresisolating the organism from affected tissues. Placingcontaminated samples in a cool environment for twoweeks may help in recovering Y. spp. Isolating avianstrains of yersinia appears to be more difficult thanisolating mammalian strains. Because there are nodemonstrable biochemical or serologic differences, ithas been assumed that avian strains are more diffi-cult to grow due to different nutritional require-ments. The most consistent isolation results havebeen obtained by placing fecal or organic material inheart-infusion broth with 5% glucose and storing thismaterial in a refrigerator for two weeks. The mate-rial is then inoculated on blood agar plates with 0.2%Tween 80 and 50 ppm tellurite and incubated at 37°Cfor two days. Yersinia causes a reduction of the tellu-rite, turning the colonies black.25

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TreatmentBirds with the peracute to acute forms of yersiniosisusually die before therapy can be instigated. Paren-teral drug administration is required if therapy hasany chance of being successful. Treating chroniccases is difficult because granulomas prevent antibi-otics from reaching the yersinia organisms nestled inthe center of necrotic debris. Flock outbreaks can beprevented by treating clinically unaffected animalsand applying strict sanitary measures.

ControlIn non-European countries where Y. pseudotubercu-losis is not endemic, repeated culture of feces duringthe quarantine period should be used to preventinfected birds from entering the country. In endemicareas, rodents and free-ranging birds can serve asreservoirs, and flock control depends on preventingthese animals from contaminating feed supplies andkeeping them out of the aviary. Several experimentalvaccines for Y. pseudotuberculosis have proven to beineffective. Feeding infected mice to toucans couldserve as a source of infection.

Y. enterocolitica is principally a human pathogen.Gulls, herons, birds of prey, crows, blackbirds andEuropean robins that inhabit areas contaminatedwith human sewage are frequently infected. Youngchildren of elementary school age are particularlysusceptible to infections.

Pseudomonas (Ps.) and Aeromonas (Ae.)

These two gram-negative rods are taxonomically un-related but nevertheless have characteristics thatmake it best from a clinical perspective to discussthem together. Both of these genera contain numer-ous species, but only Ps. aeruginosa and Ae. hydro-phila are common avian pathogens. Both bacteriaare frequently found in aquatic environments andcan propagate in cool water (20°C or lower). Bothbacteria will grow on common media and induceβ-hemolysis on blood plates. These hemolysins arepotent toxins and are capable of damaging many cellsin addition to erythrocytes. Ps. aeruginosa producesa blue-green diffusible pigment and has a sweetishodor. Ae. hydrophila causes the typical bad smell ofthe proteinolytic organisms and may be confusedwith E. coli on Endo- or MacConkey plates. Thesebacterial genera are further divided into several se-rovars and biovars. There have been insufficientstudies to divide the avian species in a similar fash-ion.

Both of these bacteria infect many mammals, includ-ing humans, as well as most of the birds that havebeen tested. Free-ranging waterfowl appear to beparticularly susceptible, but any free-ranging avianspecies that contacts contaminated food or water isprobably susceptible. Of the commonly maintainedzoo birds, penguins are very susceptible.

PathogenesisSome strains of Pseudomonas and Aeromonas pro-duce a number of extracellular toxins, includinghemolysins, elastase, protease and lecithinase, thatcause cellular damage resulting in edema, hemor-rhage and tissue necrosis. Avian strains of Ae. hydro-phila that are acetoin-producing (Voges-Proskauer-positive) are considered to be highly toxic.6 Bothspecies are principally secondary invaders. However,the toxins secreted by these organisms can be life-threatening once colonization of the host occurs. Ps.aeruginosa is resistant to many commonly used anti-biotics and can cause secondary superinfections inpatients being treated for other bacterial infections.

Clinical Disease and PathologyVirulent strains of these bacteria can cause a septi-cemia that induces diarrhea, dehydration and dysp-nea followed by acute death. Infected skin lesions areedematous or necrotizing. Localized infections mayoccur in the upper respiratory tract, causing rhinitis,sinusitis and laryngitis. Hemorrhages and coales-cent necrosis in the liver, spleen and kidney are themost common postmortem findings (see Figure 33.2).Catarrhal to hemorrhagic enteritis with edema andfibrinous inflammation of the serosal membranesmay also be noted. Histologic changes associatedwith infections include severe inflammatory reac-tions involving the venous and arterial walls. Bacte-ria are often identifiable within the lumina. Theformation of thrombi, hemorrhage and necrosis of theinfected vessels are the results.

Diagnosis and ControlThe causative agent should be isolated and identi-fied. Aviary outbreaks of pseudomonas are most com-mon when organic material contaminates the watersupply, allowing a proliferation of the organisms inthe drinking water (Table 33.3). Routine cleaning offood and water containers, along with any externalwater pipes, is an important control measure. Incu-bator contamination can be prevented by periodicallycleaning the water reservoir. Waterfowl are particu-larly susceptible to infections when water tempera-tures are above 20°C, allowing rapid proliferation of

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Ae. hydrophila. Removing waterfowl from ponds dur-ing these periods is a good control measure.

Alcaligenes (Ac.) and Bordetella (Bo.)

The genera Alcaligenes and Bordetella are taxonomi-cally related. Both genera are widely spread in theenvironment. Alcaligenes is found mainly in aquaticenvironments. Ac. faecalis, Bo. avium and Bo. bron-chiseptica infect a wide variety of birds in manyorders. Psittaciformes and turkeys as well as manyfinches seem to be particularly susceptible to thesebacteria.

There are no details on the pathogenicity of thesegenera in birds. Alcaligenes and bordetella are oppor-tunistic pathogens that potentiate viral and otherbacterial infections. Bordetella avium, a more re-cently recognized member of the genus, seems topreferentially bind to the ciliated epithelial cells ofthe upper respiratory tract.

In turkeys, combined infections of Bo. avium and theturkey rhinotracheitis virus cause the clinical andpathologic signs of rhinotracheitis. In other avianspecies, clinical signs are uncommon and, if presentat all, are nonspecific. At necropsy, tracheitis, bron-chopneumonia and air sacculitis are common find-ings with subacute to chronic courses of bordetella,whereas alcaligenes infections are characterized bycoalescent liver necrosis in addition to respiratorydisease.

DiagnosisA confirmatory diagnosis requires isolation and iden-tification of the causative agent. Serologic flock diag-nosis by means of the slide agglutination test orantibody titration by the Gruber-Widal method ispossible although no commercial antigens are avail-able.

Campylobacter (C.)

Campylobacter spp. from birds have been classifiedas: C. jejuni, the most frequent, and probably also themost pathogenic; C. coli, which is considered to beapathogenic, but is frequently confused with C. je-juni; and C. laridis, which is isolated from gulls,whose pathogenicity is still not definitely known.36

C. jejuni has incorrectly been labeled as Vibrio (usu-ally V. metschnikovii). This error has serious conse-quences because Vibrio cholerae, serotype 01 and

noncholera Vibrio can be recovered from healthybirds.

C. jejuni may appear in different forms including ashort comma, s-shaped, long spiral or coccoid form.The latter is usually an indication of degeneration.Colony formation takes 72 to 96 hours at 37-42°C ina microaerobic environment. Blood agar or selectivemedia are best for isolation. C. jejuni is relativelyunstable in the environment (surviving less than oneweek).

There are at least 50 serovars of C. jejuni.42 While thepossibility of birds serving as a source of infection formammals and vice versa has been discussed, thistransmission potential has been insufficiently stud-ied.

The host spectrum is large, and includes chickens,turkeys, pheasants, crows, gulls, ducks, geese, pi-geons, shorebirds, Pekin Nightingale, Nandu and theGreat Bustard. C. jejuni has recently been reportedin passerine birds, particularly in tropical finches(Estrildidae) and, to a lesser degree, in canaries.20

Details of occurrence and pathogenicity in manyavian species have been reported.51 Psittaciformesare susceptible, but few documented infections havebeen reported.

PathogenesisC. jejuni can be isolated from the intestinal tract ofclinically affected and asymptomatic birds. Experi-mental infections generally cause hepatitis. Factorsthat determine if an infected bird becomes clinicallyaffected have not been established. Clinical diseaseis common in birds with parasitic infections (coccidiaand nematodes), and these agents have been sug-gested as predisposing factors.

Clinical Disease and PathologyClinical signs are generally associated with subacuteto chronic hepatitis and include lethargy, anorexia,diarrhea (frequently with yellowish stained feces)and emaciation. Transmission takes several weeksthrough the flock, but spontaneous recovery and re-lapses do occur. High mortality has been noted infinches, especially among fledglings.20 Sudden deathas a result of liver rupture is possible. Heterophiliaand thrombocytophilia are the most consistentchanges in the CBC.

At necropsy the liver is enlarged, pale or greenish incolor and is congested, with or without hemorrhage.Perivascular infiltrates make the lobules appearmore prominent. Coalescing necrotic hepatitis is a

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common histologic finding. Catarrhal enteritis (alsohemorrhagic enteritis in pheasants, turkeys, Teng-malm’s Owl and coot) has been described. In gulls,erosion of the ventriculus has been reported.

DiagnosisDiagnosis requires isolation of C. jejuni from affectedtissues. Phase-contrast microscopy of bile to demon-strate suggestive organisms may provide a tentativediagnosis. Fecal samples can be used for culture inlive birds. A transport medium is necessary to ensuresurvival of the organism.

Treatment and ControlThere are discrepancies between the antibiogramsand clinical recovery. Erythromycin or tetracyclines,dehydro- or streptomycin (never in Psittaciformes) orfurane derivatives (not in waterfowl) can be tried.Diseases frequently recur despite therapy. Thoroughcleaning and disinfecting of the aviary may helpprevent reinfection. Dogs can be a reservoir for hu-man infections, but it is not known if they can trans-mit the organisms to birds. Dogs should not be al-lowed direct access to birds.

Vibrio (V.)

The genus Vibrio comprises numerous species thatare not easy to differentiate. V. cholerae is of utmostimportance as a zoonotic organism. In birds, espe-cially in gulls, V. cholerae (serovar 01) is demonstra-ble in the intestinal tract, although no clinical orpathologic signs have been described. Numerousother V. spp. are collectively designated NAG (= non-agglutinable), because they do not agglutinate withhuman cholera antiserum. NAG strains can be iso-lated from the feces of many bird species, particu-larly waterfowl (vibrio is generally found in aquatichabitats).4 NAG vibrios have not been documented asa cause of clinical disease in any avian species. Be-cause some NAG strains can cause a mild intestinaldisease in humans, an analysis of avian strains in thevicinity of human cases might be advisable.

Spirochaetaceae

Borrelia (Bor.) anserina (syn. Spirochaeta gallina-rum) is a gram-negative, helical motile organism thatstains with Giemsa. A granular form of the organismmay occur in ticks and the blood of the birds thathave recovered from a disease. The host spectrumincludes geese and ducks, turkeys, chickens, pheas-ants, grouse, partridges, pigeons, crows, magpies,House Sparrows, starlings and African Grey Parrots.

TransmissionThe main vectors for transmission are ticks, in whichthe organism can be passed transovarially and sur-vive for over a year. Mosquitoes and other bitinginsects play a minor role in transmission. Transmis-sion from bird to bird by excreta is of minor impor-tance epizootiologically.

PathogenesisYoung chicks (one to three weeks of age) are particu-larly susceptible. Adults may also be infected. Bor. isin the peripheral blood from the fourth to the ninthday post-infection and remains in the blood approxi-mately seven days. The organism can then be foundin parenchymal organs for another 30 days. Deathmay occur from embolism due to agglutinating borre-lias. A strain-specific immunity develops in survi-vors. Incubation periods are four to eight days de-pending on the species of ticks.

Clinical Disease and PathologyAcute cases are characterized by a high fever (bacte-ria generally cause a low body temperature), ano-rexia, depression (droopy, cyanotic heads), yellowishdiarrhea, lethargy, ataxia and paralysis. Morbidity ishigh, and mortality may range from 10 to 100%depending upon the susceptibility of the host. Spon-taneous recovery may occur around the sixth daypost-infection. Chronic disease is characterized byanemia, paralysis and dyspnea.

The albumin fraction in the serum decreases to 37%and an increase of the aspartate aminotransferase isaccompanied by a decrease of the alkaline phos-phatase, the total lipids and the cholesterol.

At necropsy, a mottled, severely enlarged liver ischaracteristic except in pheasants. In these birds thespleen may be small or normal in size.58 The livershows hemorrhages and necrotic foci. Mucoid hemor-rhagic enteritis, serofibrinous pericarditis and swol-len kidneys may also be seen. Histology displaysmultiple necrotic foci without inflammatory reac-tions. Bor. can be demonstrated by argentation.

DiagnosisBlood smears stained with Giemsa or examined bydarkfield microscopy are useful for diagnosis. Cultur-ing Bor. sp. is very difficult. Antibodies (agglutina-tion, fluorescence techniques, immunodiffusion) canbe demonstrated from the 4th to the 30th day post-infection.

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Treponema (T.) spp.: Treponema spp. are helicalmotile organisms that are much smaller than Spiro-chaeta spp. An unclassified Treponema sp. (0.5 µmwide with 13 to 15 flagella)12 is the cause of a watery,intermittent typhlitis in chickens. The organism isantigenically related to but distinct from T. hyodysen-teriae. Chickens are the only defined host and loseweight in response to a malabsorption syndrome.12,22

Histopathology shows an increased number of gobletcells in the cecal mucosa, focal epithelial desquama-tion and many Treponema organisms in the smallfissures of the epithelium. The incubation period isone to seven weeks dependent on the infective dose.Culture is possible on spectinomycin blood agar in ananaerobic atmosphere. Fluorescent antibodies de-signed for T. hyodysenteriae can be used to demon-strate the organisms in affected tissue.

Spirochaetaceae Undifferentiated: A non-classifiedspirochete from choanal and tracheal mucus of acockatiel has been described. The organisms were 0.3to 0.4 X 10 to 15 µm in size and occurred in largenumbers on the mucosa. Two other cockatiels havebeen found to harbor similar organisms in the respi-ratory passage. Histopathology showed a mild in-flammatory reaction in the nasal sinus, but not in thetrachea. In the lower parts of the respiratory tract,the organisms could not be demonstrated using ar-gentation. The significance of these findings is un-known. Interference with the ciliary activity of therespiratory mucosa is conceivable.65

Spirochetes were demonstrated in a pharyngealswab of a cockatiel that was depressed and sneezing.The bird had spent ten minutes with another cocka-tiel that was showing similar clinical signs ten daysbefore being presented for evaluation.

Pasteurella (P.)

The family of Pasteurellaceae currently includes thegenera Pasteurella, Actinobacillus and Haemophi-lus.49 All three genera can be pathogens in birds.

Pasteurella characteristically exhibit bipolar stain-ing in tissue smears or from first culture passageswhen fixed in methanol and stained with methyleneblue. There are presently eleven species within thisgenus, but others will undoubtedly be added. P. mul-tocida, which causes fowl cholera, and P. gallinarumare two of the most commonly encountered species.The latter is usually considered a secondary patho-gen. Some of the Pasteurella organisms isolated fromwaterfowl, pigeons and Psittaciformes have not been

taxonomically classified. Some isolates designated P.haemolytica (gram-negative, polymorphic rods) areimproperly classified and do not belong in this genus.The characteristics of these strains resemble those ofthe genus Actinobacillus. Reports on isolation of P.pneumotropica from birds are questionable. This spe-cies appears to be host-specific and is found in rats orother rodents. Similarly, P. ureae is believed to behost-specific for humans.

Pasteurella has been associated with disease in Pha-sianiformes, Anatiformes, Psittaciformes, Columbi-formes and Passeriformes. There is variance in spe-cies susceptibility. The clinical presentations andpathomorphologic changes are similar to those de-scribed for yersiniosis. Propagation outside the hostcan occur but requires very specific conditions oftemperature, relative humidity and pH. Such condi-tions may occur in large bodies of water, and in thesesituations Pasteurella spp. can survive for long peri-ods. Epornitics are most common in the northernhemisphere from November to December. Outbreaksin tropical climates peak with seasonal highs in am-bient temperature and humidity.

P. multocida: The etiologic agent of fowl cholera, thespecies is divided into strains based on 16 serologi-cally distinct endotoxins and 4 capsular polysaccha-rides. Serotypes 1 and 3 and capsule types A and Dare most commonly isolated from birds. Three sub-species, P. multocida (m.) multocida, P. m. galli-narum and P. m. septica, have been distinguishedbased on differences in virulence. The latter is con-sidered to be the most virulent.

P. pneumotropica is indigenous in rodents and occa-sionally causes disease in aviary birds and pigeons.Infected birds develop pneumonia and may exhibitdyspnea shortly before death. Detailed informationon the pathogenesis and clinical progression of P.pneumotropica in companion birds has not been re-ported.

P. gallinarum appears to have a similar host spec-trum as P. multocida; however, P. gallinarum isthought to be much less pathogenic. If the organismis able to colonize the respiratory mucosa, it caninduce conjunctivitis and respiratory signs includingcoryza, rales and dyspnea. P. gallinarum has beenisolated from the choanae and nostrils of Psittacifor-mes with concomitant Aspergillus spp. infections inthe lungs and air sacs. Aspergillosis is one of thetriggering factors that allows this secondary patho-gen to overcome host defenses. Postmortem findingsassociated with P. gallinarum include catarrhal to

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fibrinous inflammation of the upper respiratorytract, pneumonia and air sacculitis.

TransmissionPasteurella infections in birds principally occur inthe respiratory tract. Asymptomatic carriers harborthe bacteria in the nasal cavities, sinuses and cho-anae. Transmission can occur through direct contactwith contaminated aerosols or through mechanicalvectors such as blood-sucking mites. Infected rodentsand free-ranging birds are considered important res-ervoirs. Pasteurella is shed almost exclusively fromthe upper respiratory tract. Shedding in the feces israre, and egg transmission has not been documented.P. multocida is a common inhabitant of the oralcavity of some carnivores, particularly cats, and sep-ticemic infections can occur through bite wounds.Cats should always be considered to be carriers of P.multocida, and any bird that has been mouthed by acat should be treated with antibiotics immediately(Figure 33.5).40

PathogenesisVirulent strains of P. multocida cause an acute septi-cemia and death. Less virulent strains result in bac-teriemia and colonization of the lungs, liver, kidneys,spleen and heart. Weakly virulent strains generallycause a chronic respiratory disease. The endotoxins

produced by Pasteurella damage blood vessels, caus-ing edema, hemorrhage and coagulation necrosis,particularly in the liver. Diseases by less virulentstrains usually occur in stressed or immunocom-promised hosts.

Clinical Disease and PathologyAcute forms are characterized by cyanosis, dyspneaand diarrhea followed by death. Excess mucus maybe present around the nostrils or beak. Birds thatsurvive acute disease often develop respiratory rales,sinusitis, conjunctivitis or swelling of the sinus in-fraorbitalis. Arthritis and CNS signs have been re-ported in some chronic cases. Granulomatous derma-titis has been noted in raptors, owls and pigeons.

Postmortem findings with acute disease may be ab-sent or limited to petechiae or ecchymoses of theparenchymal organs. Prolonged cases are charac-terized by exudative serositis (mainly white, in con-trast to yellow with E. coli) and the formation ofnecrotic foci in infected organs. Catarrhal to fibri-nous rhinitis, necrotic pneumonia, sinusitis, ble-pharoconjunctivitis and tracheitis are common withchronic courses. Following bacteremia, Pasteurellamay colonize numerous tissues, resulting in arthri-tis, osteomyelitis, otitis media and granulomatousdermatitis. Granulomas may also be noted in theliver and spleen. Some strains will colonize the aircells of the cranial bones causing fibrinous exudate.In waterfowl, a diphtheroid enteritis may be ob-served. Histologic changes are nonspecific.

DiagnosisThe isolation of the causative agent is necessary. Theoccurrence of Pasteurella spp. in a flock can be deter-mined through serology using immunodiffusion orindirect hemagglutination tests. Unfortunately, com-mercial antigens for these tests are not available.Serotyping and differentiation of the subspecies re-quire specialized testing.

TreatmentSepticemic birds rarely survive, even when treatedintensively. Parenteral administration of broad-spec-trum, long-acting sulfonamides can be tried. Thecombined use of antibiotics and hyperimmune serumhas proven to be beneficial. Treating birds withchronic forms is very difficult because of the irre-versible damage that occurs to parenchymal organs.

ControlPreventing rodents and free-ranging birds from en-tering the aviary is important in preventing infec-

FIG 33.5 The hallmark sign of bacterial septicemia is depression.Birds that are bitten or scratched by cats frequently develop P.multocida bacteremia. Affected birds may appear normal immedi-ately after the injury occurs, and become rapidly depressed and die12 to 24 hours later. Any carnivore-related injury in a bird is acritical emergency.

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tions. Vaccines for P. multocida are commerciallyavailable, but their effectiveness is poor. Failuresassociated with the vaccine occur because of the nu-merous different serotypes and the fact that endotox-ins are more immunogenic than the bacterial cap-sule. The production of vaccines from strains thatpersist in an aviary may provide successful long-term control.

Actinobacillus (At.)

The genus Actinobacillus consists of a group of organ-isms provisionally differentiated into more than 20biovars, some of which have a rather high host speci-ficity. The taxonomic reclassification of the Pas-teurellaceae is intertwined with the genus Actino-bacillus. Because of these classification revisions,even the actinobacilli that are pathogenic in birdshave not been named. The situation has been compli-cated in recent years because many new strains havebeen isolated from Psittaciformes, Columbiformes,Anatiformes and Fringillidae. One biovar has beenreferenced in the literature as P. haemolytica syn. At.salpingitidis. However, this classification is notvalid. The knowledge of the biology and pathogenic-ity of the members of the genus is limited.

Actinobacilli are polymorphic rods that may exhibitbipolar staining similar to Pasteurellae. Most strainsgrow only on blood agar plates or media containingserum. Some strains, particularly of At. salpingi-tidis, hemolyze avian and bovine erythrocytes or pro-duce exotoxins that are capable of causing arteritis.Some strains are considered to be primary patho-gens, but the majority of this genus is comprised ofopportunistic organisms. There are no simple labora-tory tests for differentiation between primary andsecondary invaders.

There is little information on routes of transmission.It has been proven that egg transmission of somestrains occurs in chickens and geese. Incubation pe-riods in the avian host are not known.

Clinical Disease and PathologyMany infected birds die acutely. Birds with a morechronic course typically develop joint lesions. Spe-cies-specific strains that infect geese morphologicallyresemble P. influenzae. This organism has been ref-erenced as a cause of chronic disease in the gosling,26

characterized by emaciation, failure to thrive, poorfeed conversion and arthritis. Egg transmission maycause reduced hatchability. Asymptomatic infectionsare thought to occur in adult breeders, with clinical

signs developing in goslings each season. At necropsy,liver necrosis, salpingitis, peritonitis, endocarditisvalvularis and fibrinous arthritis are typical lesions.In young geese, polyserositis and arthritis are promi-nent.

Diagnosis and Treatment Isolation and identification of the causative agent isnecessary for diagnosis.

E. coli and other bacteria, particularly anatipestiferinfections in waterfowl, have to be considered ascausative agents for the salpingitis, peritonitis andpolyserositis.

Tetracyclines and chloramphenicol are indicated forinitial therapy. Sensitivities for many strains aredifficult to interpret because of oversized inhibitionzones. In young geese, antibiotics must be givenduring the first week of life or lesions become tooextensive to be reversed.

Haemophilus (H.)

The haemophilus strains that infect companion birdshave not been properly classified. Chickens are con-sidered to be the only definitive host of H. paragalli-narum, which is the agent of coryza contagiosa galli-narum. Experimentally, Columbiformes andAnatiformes are resistant to infection. SeveralHaemophilus spp., including H. avium an d H.paravium, can be isolated from birds with coryza;however, their involvement in the disease process isquestionable. They probably serve as secondary in-vaders that sustain upper and sometimes lower res-piratory tract disease.11,35

PathogenesisDetails on the pathogenesis of Haemophilus spp.strains that infect Psittaciformes and Columbifor-mes are scarce. H. paragallinarum is known to pro-duce a number of cellular toxins, including neu-raminidase, nitratase and catalase. Birds do notappear to develop an immune response followinginfection, and relapses are common.

Clinical Disease and PathologyHaemophilus infections generally cause a rhinitisthat results in a serous-to-mucoid or even fibrinousexudate. Conjunctivitis and sinusitis may also occur.The most common postmortem finding is catarrhal-to-fibrinous rhinitis. Bronchopneumonia and air sac-culitis are frequently described but are usually theresult of concomitant infections (virus, other bacte-

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ria, Candida spp.). For those lesions supposedlycaused by Haemophilus spp. apart from H. paragalli-narum see Table 33.4.32,35 Histopathology reveals un-characteristic lesions.

TABLE 33.4 Clinical Disease Caused by Haemophilus in Avian Species

Blue Crane Pneumonia (together with staphylococci)and necrosis of liver tissue

Pigeon Rhinitis

African Grey Parrot Pneumonia, air sacculitis

Plum-headed Parakeet Sinusitis, swelling of the liver togetherwith E. coli or related organisms

Eastern Rosella Sinusitis, swelling of the liver togetherwith E. coli or related organisms

Budgerigar Rhinitis (possibly together with Pasteurella or E. coli)

Muscovy Duck Rhinitis, sinusitis

Andean Goose Rhinitis, hemorrhage, jejunitis

Turkey Sinusitis, air sacculitis

Golden Pheasant Sinusitis, diphtheroid surface lining ofthe beak cavity

Siamese Fireback Necrosis of the lung tissue.

Other Gram-negative Rods

New Duck Disease (Duck Septicemia)

The etiologic agent of duck septicemia has been sus-pected to be Pfeifferella, Pasteurella or Moraxellaanatipestifer. The causative organism has recentlybeen placed in the genus Cytophaga, which is asemiaerobic, nonmotile rod.49 The genus contains atleast 19 serovars; serovars 1-3 are most common inEurope; serovars 1, 2 and 5 are most common in theUnited States; serovar 3 is frequently isolated inAustralia. This organism is known to infect ducksand geese, free-ranging waterfowl, turkeys, pheas-ants and Psittaciformes. There is no information onits virulence or ability to survive in the environment.

Experimental disease does not occur following oraladministration, and the respiratory tract is thoughtto be the primary portal of entrance to the host. Eggtransmission resulting in high morbidity and mortal-ity of ducklings is a substantial factor for the flock.

The pathogenicity of cytophaga is undetermined. Un-doubtedly, there are strain differences in virulence,

and the condition of the host must also play a role.The incubation period in ducks ranges from three toten days.

Clinical Disease and PathologyInfected ducklings (two weeks of age) usually dieperacutely. Mortality rates in this age group canreach 75% of exposed young. Acute disease developsin older birds and is characterized by sinusitis, con-junctivitis, coughing and diarrhea, followed in twodays by tremors, ataxia and convulsions. Survivorsare stunted and fail to grow. Fibrinopurulent polyse-rositis is the characteristic postmortem finding.Other changes include lung congestion, hepa-tomegaly, splenomegaly, pericarditis and perihepati-tis. Cytophaga-induced spondylitis with compressionof the spinal cord was reported in turkeys.10 Diffusefibrinous meningitis with lymphocytic infiltrationaround the meningeal blood vessels was a charac-teristic histologic lesion. There was exudate forma-tion within the ventricles as well as proliferation ofmicroglia in the subpial and periventricularsystem.

DiagnosisThe occurrence of polyserositis is highly suggestive ofan infection. Isolation and identification of the causa-tive agent is necessary in all other cases. An ELISAcan be used to survey a flock for serologic response.

Tularemia

Tularemia is caused by Francisella tularensis, a mo-tile, short rod, 0.2 X 0.3-0.7 µm in size. Isolates arereported occasionally, mainly from birds that inhabitthe northern and subarctic regions of the northernhemisphere, such as the Common Pheasant, Wax-wing, Ural Owl, Rough-legged Hawk and CommonRaven. Rodents are considered to be the primaryreservoir. Nothing is known about the clinical signs.The pathology resembles that of Pasteurella orYersinia infections. Francisella previously has beenclassified with these two genera. The organism isconsidered to be a zoonotic agent.

Acinetobacter calcoaceticus (An.)

This organism forms either cocci (fresh culture) orrods. It grows on commonly used media, even onsome selective media for Enterobacteriaceae. Thehost spectrum is wide, and many avian orders canharbor the organism in the respiratory or intestinaltracts. Egg transmission is possible in many avianspecies. No reports conclusively describe consistently

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occurring lesions in any avian species. Therefore, itis assumed that the organism has a low pathogenic-ity, and infections indicate a compromised host.

Gram-positive Bacteriaof Clinical Significance

Staphylococcus (S.)

Staphylococcus infections can induce sporadic or en-zootic disease in many avian species. Clinical mani-festations may include acute septicemia or subacute-to-chronic arthritis, osteomyelitis and osteitis. Lesscommon clinical problems include vesicular dermati-tis or omphalitis. Staphylococci, particularly S.aureus, can function as primary pathogens or maycomplicate other infections as secondary invaders.

Isolation of the staphylococci is relatively simple us-ing common media and growth conditions. Taxonomyliterature50 currently lists 21 Staphylococcus spp., 14of which can be found in birds and are given here inorder of decreasing frequency. S. xylosis is consideredalmost apathogenic. S. sciuri and S. lentus (the lattera former biovar of S. sciuri) have some pathogenicitymarkers. S. aureus includes more virulent strainsthan any other species. These four Staphylococcusspecies are further divided into several biovars. Be-cause some of these biovars are recovered only in alimited number of closely related bird species, theymay represent bacterial organisms that haveadapted to specific hosts. Other less commonly iso-lated species include S. intermedius, S. hyicus, S.cohnii, S. saprophyticus, S. haemolyticus, S. warneri,S. hominis, S. epidermidis, S. gallinarum and S.capitis. S. epidermis was frequently cited in earlierliterature but, using current diagnostic tools, is todayrarely found in birds. The isolation of these lesscommon species frequently depends on the internalor external environment of the patient, and limitedinformation is available concerning their pathogenic-ity.

Staphylococci have several pathogenicity markersincluding production of the clumping factor, hemolys-ins, DNase, phosphatase, protein A and leuko-cidine. The presence of the clumping factor seems tocorrelate closely with pathogenicity in avian pa-tients. Other pathogenicity markers have not been

studied sufficiently to determine their importance inbirds. Staphylococcus protein A, which is found in thebacterial cell wall, is capable of binding to the Fc-fragment of immunoglobulin, thereby inhibitingphagocytosis of the organism. The correlation be-tween protein A production and the virulence ofavian Staphylococcus strains is poorly documented.

Members of the genus Staphylococcus (apart from S.aureus) are commonly recovered from many avianspecies and are considered part of the autochthonousflora. When present in diseased tissue, they are gen-erally considered to be secondary invaders. BecauseS. aureus includes the most virulent strains, thefollowing discussion applies mainly to this species.

S. aureus

Avian strains of virulent S. aureus are relativelyspecies-specific and rarely induce disease in mam-mals. The organism is found in abundant quantitiesin air and dust. Isolation of the organism can fre-quently be accomplished from the skin and the mu-cosa of the respiratory or digestive tract of clinicallynormal birds (Figure 33.6). S. aureus, like otherStaphylococcus species, is relatively stable in theenvironment and can remain infectious for long peri-

FIG 33.6 A five-year-old Amazon parrot was presented with anacute onset of picking at the feet and legs, which caused hyperemiaand scab formation. This syndrome, called Amazon foot necrosis,has been reported in Amazona spp., and Staphylococcus spp. arefrequently isolated from the lesions. However, staphylococci arepart of the autochthonous flora and are probably not the primarycause of this problem. This affected Amazon parrot belonged to aclient who smoked, and when the owner started washing her handsafter smoking (presumably to remove nicotine sulfate, a potenttoxin), the foot and leg lesions resolved. The client eventuallystopped smoking and the bird had no further episodes of Amazonfoot necrosis.

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ods of time outside the host. Given proper conditions,the organism can propagate in an external environ-ment. Like many bacteria, Staphylococcus can alsodevelop resistance to disinfectants following continu-ous exposure, and frequent changing of disinfectantsis required to prevent the development of resistantstrains.

Techniques for differentiating between avian andmammalian strains of S. aureus remain unsatisfac-tory. Evaluating the type of lesions caused by experi-mental subcutaneous infection of S. aureus in birdsmay prove valuable in differentiating between avianand mammalian strains.

PathogenesisThe importance of Staphylococcus infections in birdsis clinically underestimated. Individual strains maycause clinical problems in one bird while being con-sidered normal autochthonous flora in another. Lipo-teichoic acid, a major component of the staphylococ-cal wall, is instrumental in the specific capacity ofthis organism to bind to host cell receptors, particu-larly in the respiratory system. Such binding is aprecondition for colonization and subsequent infec-tion. However, avirulent strains can also bind to thesame receptors and may compete for receptor sites,preventing colonization of virulent strains. Thisprocess is called “bacterial interference.” Suitablestrains of Staphylococcus have been used as prophy-lactic tools, especially in poults. Some of theseapathogenic strains also produce bacteriocin, whichcan inhibit the growth of a variety of bacteria.

Although endogenous infections can be primary, theyare frequently secondary to respiratory tract coloni-zation and progress to septicemia. If an infected birdsurvives the acute septicemic stage of the disease, itwill typically develop localized changes. Focal lesionsoccur as a result of thrombi formation in the arteri-oles and capillaries, which leads to ischemic necrosis.Clinically, these necrotic areas are frequently local-ized at the tips of the extremities and in the skin. Inaddition, infarction can also cause necrotic lesions ininternal organs, particularly the liver and kidneys,which are more difficult to discern clinically. Thecentral nervous system (CNS) is another site proneto Staphylococcus-induced lesions. Postsepticemicdevelopment of arthritis, tenovaginitis, osteitis andosteomyelitis followed by chronic skeletal changesare considered together as one disease process (Fig-ure 33.7). These problems usually occur after a four-to seven-day period of septicemia.

Exogenous infections usually result in localized skindisease, although subsequent septicemia can occur insome cases. Birds, unlike mammals, are generallyresistant to wound infection. To become established,exogenous bacteria typically require epitheliumdamaged by other infectious agents (particularlyclostridia or poxvirus), immunosuppression (includ-ing immunosuppressive viruses such as retrovirusesor reovirus), environmental stressors or prolongedapplication of an antibiotic.

Localized problems associated with Staphylococcusspp. can also result from a delayed hypersensitivityreaction. This type of response is considered to be oneof the major factors in treating staphylococcus-re-lated bumblefoot.

Clinical Disease and PathologyStaphylococcus can induce a wide range of clinicaland pathologic lesions, including high embryonicmortality, yolk sac or umbilical inflammation, septi-cemia, arthritis-synovitis, osteomyelitis, vesiculardermatitis, gangrenous dermatitis and bumblefoot.

Endogenous infections usually cause internal le-sions, while exogenous infections frequently result indermatitis and bumblefoot. Staphylococcal lesions inthe umbilical region are typically either dry andbrownish or smudgy, reddish and edematous. Clini-cal problems are most common in newly hatchedchicks (up to ten days of age), in which the yolk sacin the body cavity is not absorbed normally, withpossible decomposition of its contents.

Staphylococcus septicemia may be characterized bynonspecific clinical signs including lethargy, ano-rexia, a kyphotic posture, ruffled plumage and sud-den death. The acute occurrence of necrosis to thedistal digits or adnexa of the head and neck is sug-gestive of a thrombi-inducing infection, which can bea sequela to staphylococcus septicemia. During theinitial phases of the ischemic process, the involveddigits may be swollen, congested and painful, andmany affected birds exhibit lameness. The acute on-set of tremors, opisthotonos and torticollis can oftenbe linked to staphylococcus-induced necrosis in theCNS. Gross lesions associated with staphylococcussepticemia include petechiae and ecchymoses of in-ternal organs. Chronic infections may result in endo-carditis valvularis. Histologic changes vary with theclinical course of disease but typically consist of aheterophilic and granulomatous response.

Arthritis-synovitis, characterized by the formation ofserofibrinous or fibrinous inflammation of the

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synovial membranes of tendon sheaths and articularbursae, is frequently noted with staphylococcal infec-tions in gallinaceous species. Any joint may be in-volved but there appears to be a predilection forcolonization of the tarsal and metatarsal joints. Fol-lowing antibiotic therapy, staphylococcus may be pre-sent in its unstable L-form, which is difficult to treat.

In immature birds with active growth plates, Staphy-lococcus frequently localizes in the epiphyseal areawith secondary invasion of the bone marrow, result-ing in osteomyelitis. Endogenous osteomyelitis isconsidered to be impossible after consolidation of thegrowth plate.46 Infection of the growth plates oftenleads to chronic skeletal abnormalities. Infectionsare frequently localized to the proximal epiphyses ofthe femur, tibiotarsus, tarsometatarsus and fifth toseventh thoracic vertebrae. Vertebral injury maylead to clinical changes described as “kinky back”(Figure 33.8). Swelling and colliquation associatedwith the infection cause deformation of the vertebralspongiosa, which may lead to narrowing of the verte-bral foramina and compression of the spinal cord.

Staphylococcus-induced vesicular dermatitis is char-acterized by the formation of vesicles containing yel-lowish exudate that form brownish to blackish crustsfollowing rupture. Concomitant infection with poxvi-

rus (or other immunosuppressive agents) may beinvolved in the disease process. Histologic evaluationof biopsy samples is required to confirm an underly-ing poxvirus.

Staphylococcus-induced gangrenous dermatitis is in-itially recognized by the occurrence of subcutaneousedema and hemorrhage followed by inflammation ofthe skin. Affected skin is typically blackish andsmudgy and feather loss is common. Clostridiumperfringens or another Clostridium sp. is a commonsecondary invader. Both Staphylococcus and Clos-tridium require a triggering factor (often damagedepithelium) to enter the tissue. Gangrenous derma-titis is rare in most bird species.

Advanced bumblefoot is a necrotizing abscess on theplantar surface of the foot. Depending on the locationand chronicity of the abscess, infection may or maynot extend to neighboring joints, tendon sheaths andbones. The condition is frequently described in rap-tors but may occur in other avian species. The precisepathogenesis of bumblefoot is undetermined (seeChapter 16). Although staphylococci are frequentlyisolated from these lesions, they are by no means theonly bacteria that can be recovered from diseasedtissue. Systemic infections that result in other le-

FIG 33.7 Staphylococcus spp. can cause osteomyelitis either secondary to septicemia or following an injury that allows colonization of thebone. Chronic osteomyelitis, as demonstrated in this radiograph, typically requires surgery to remove necrotic tissue and long-termantibiotic therapy, preferably with clindamycin because of its high affinity to bone and bone marrow.

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sions or death can occur secondary to bumblefootcaused by virulent strains of S. aureus.

DiagnosisStaphylococcal colonies, like Micrococcus spp., haveopaque pigments (from white to yellow). Clumpingfactor-positive strains are likely to be virulent, andrequire an aggressive therapy based on antibioticsensitivities.

Serologic diagnostic techniques using agglutinins,antihemolysins or antitoxins are of little value indiagnosing staphylococcosis. Cross-agglutinins, par-ticularly against Salmonella gallinarum-pullorum,frequently result in false-positive reactions.

Streptococcus (Sc.) and Enterococcus (Ec.)

Streptococci and enterococci consist of numerous spe-cies that readily grow on most commonly used media.Differentiation between the species is based uponmorphologic, biochemical and serologic charac-teristics. These organisms are ubiquitous (mainly in

dust and air), and some strains can survive for longperiods in the environment. They are sensitive tomost commonly used disinfectants.

Sc. and Ec. are considered part of the autochthonousflora of the skin and the mucosal surfaces of thedigestive, respiratory and reproductive tracts. Sc.and Ec. transition from normal flora to disease-in-ducing agents depends on the functional state of hostdefense systems. Predisposing factors to disease in-clude immunosuppression, concomitant infectionsand exposure to a variety of toxins and pathogenicityfactors that may be produced by some strains of Sc.and Ec.

The ß-hemolyzing, pyogenic streptococci, frequentlyfound in mammals, are rare in birds. In comparison,α-hemolyzing streptococci are quite common. It hasbeen suggested that most of the latter species shouldbe included into the newly established genus Entero-coccus.45,54 Enterococci are less fastidious than strep-tococci, and many will grow on selective media usedfor isolating Enterobacteriaceae. Numerous species

FIG 33.8 An eight-week-old African Grey Parrot was presented for an inability to stand or ambulate properly. On physical examination,the bird was BAR, in excellent weight (325 grams) and had a palpable spinal deformity. Radiographs indicated scoliosis. Bacterial infectionsincluding Staphylococcus spp. can cause spinal deformities. In this bird, the WBC was normal and the etiology of the problem wasundetermined. Congenital abnormalities appear to be particularly common in African Grey Parrots and may have been the cause of thisscoliosis.

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of streptococci and enterococci havebeen isolated from birds.15,16,17,29

References to the pathogenicity ofseveral Sc. spp. vary. Variance in theobserved behavior of these opportun-istic organisms may be a result of theeffects induced by concomitant viralor chlamydial infections, the lack ofexperimental infections and confu-sion in taxonomy or nomenclature.Irrespective of predisposing factors,many Sc. and Ec. strains producecompounds that facilitate an infec-tion (M-protein, capsules) or produceextracellular substances that inhibitthe host defense system (hemolysinS, streptolysin S, hyaluronic acid,streptokinase, DNase, NADase andesterases) or inhibit other competingbacteria (bacteriocins).

Vertical transmission (including L-forms) can be a cause of early embryonicdeath and post-hatching develop-mental problems (Figure 33.9). Infec-tions in hatchlings are usually asso-ciated with omphalogenic postnatalsepticemia.

PathogenesisThe rarely occurring Sc. spp. group C can cause asepticemia followed by an embolic-thrombotic sys-temic disease and death, usually in adult birds. Fol-lowing infection, hematogenic and intrahepaticspreading results in colonization in almost all organsif the host survives (probably agent- and host-spe-cific). In experimental infections, a persistent bac-teremia has been described, the duration of whichcan range from weeks to months. In addition to thepathogenicity factors already mentioned, Sc. group Cmay also produce reagins that govern the host reac-tions. Genetic and environmental factors as well asconcurrent viral infections or immunosuppressionsmay predispose mainly adult birds to this rare infec-tion.

Little information is available on the pathogenesis ofSc. pneumoniae or Sc. pleomorphus lesions in birds.Sc. bovis has been described as a pathogen in pi-geons17 and ducks;52 however, the pathogenesis ofthese infections is unclear.

Enterococci outside of the digestive tract can causenecrotizing inflammatory lesions in infected organs.

However, the pathogenicity of Ec. spp. is generallylow. Experimental infections indicate that diseaseinduction requires predisposing immunosuppressivefactors. As a rule, natural infections occur by the oralroute and are most common in postnatal and growingbirds.

Ec. faecalis can induce an acute septicemic or a sub-acute-chronic disease. The acute form predominatesin young birds, and survivors often develop endo-carditis. Details on pathogenesis are known only ingallinaceous species. Sc. faecalis is thought to play acentral role in the malabsorption syndrome de-scribed in chickens.

Egg transmission of Ec. faecalis (also as an L-form)is associated with an acute post-hatching septicemia.The subclinically infected yolk sac is thought to bethe source of disease in the hatchling. Ec. faecalis isnot considered autochthonous flora of canaries andmay cause a primary respiratory disease in this spe-cies.18 Subacute-to-chronic tracheitis with dyspneaand rales are considered natural components of thedisease. Ec. cecorum has not been associated withdisease in experimental infections.14 Ec. columbae ismainly found in pigeons and constitutes a componentof the autochthonous intestinal flora.

FIG 33.9 Bacterial infections (Streptococcus, Staphylococcus, Enterococcus and Salmo-nella spp.) of the egg can cause embryonal death, post-hatching developmental problemsand yolk sacculitis.

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Clinical DiseaseThe clinical diseases caused by pyogenic streptococciand other streptococci and enterococci are relativelysimilar. Clinical presentation can be peracute tochronic, with birds surviving six to eight weeks in thechronic form. Omphalitis in recent hatchlings is typi-cal with egg transmission or infections obtained fromthe hatchery.

An Amazon parrot with a slight nasal discharge wasfound to have a Sc. group G infection that was caus-ing chronic respiratory disease in the children of thehouse. Presumably, the bird was infected by the chil-dren.

Septicemia may lead to a peracute apoplectiformdeath or severe depression followed by death in twoto three days. Other signs such as diarrhea, dyspnea,paresis, conjunctivitis and sinusitis (Japanese Quail)may develop.

Chronic disease is typified by inflammation of joints,tendon sheaths and adnexa of the head. Fibrinousjoint lesions, with or without abscess formation, canoccur several months after the initial infection. Birdsthat survive systemic infections may develop cardiacvalve insufficiency secondary to endocarditis. Thiscondition is difficult to diagnose and often presentsas chronic dyspnea.

Sc. pyogenes has been associated with bacteremia inthe Humboldt Penguin, White Pelican, and severalPsittaciformes, Anatiformes and Phasianiformes. Ithas not been clearly defined whether the bacteremiain these cases was a result of true group A strepto-cocci, or whether the inciting strain was Sc. pyogenesanimalis (classified in group C). Group C Streptococ-cus has been associated with pneumonia secondaryto bacteremia in a variety of avian species. In theostrich, Sc. group C cases are characterized by akine-sia, anorexia and dysphagia. This organism togetherwi t h Corynebacterium pyogenes c an i nd ucediphtheroid lesions in the mucosa of the beak cavityand the crop that can result in similar clinical signs.32

Sc. bovis infections in pigeons have been associatedwith clinical changes ranging from peracute death tochronic lameness (myositis) and arthritis.

Ec. group D is frequently implicated as a cause ofpneumonia in various bird species, particularly Pas-seriformes, and primarily infects young birds. In ca-naries, Ec. faecalis can cause a tracheitis and chronicrespiratory disease that manifests clinically aschanges in the voice (more “sparrow-like”) or com-

plete voice loss. Tracheal mites (Sternostoma tra-cheacolum) can cause similar clinical signs in thisspecies. Epidemiologically, the infection spreadsslowly through the whole flock. Some affected birdsdevelop dyspnea and die, while others may temporar-ily recover. Relapses are common in recovered birds.

PathologyGross lesions in birds that die acutely with bacter-emia include subepicardial and myocardial hemor-rhages and serofibrinous polyserositis. The subcuta-neous tissues, serosal membranes and pericardiummay be congested, and the spleen is frequently hy-perplastic. Lung congestion, pneumonia or petechia-tion of the laryngeal and tracheal mucosa may benoted in some species. The liver may be slightlyswollen and exhibit a greenish discoloration. Ca-tarrhal enteritis, skeletal muscle hemorrhages andswollen kidneys may also be observed. Muscle ne-crosis and purulent myositis are frequently describedin pigeons with Sc. bovis infections.

Pathologic changes in chronic cases are charac-terized by arthritis with a light, mucoid exudate andthe formation of coagulated or dried exudates in thebody cavity. Cauliflower-like or granulomatousatrioventricular inflammation may develop, particu-larly on the left cardiac valve. Pyogenic streptococcimay cause chronic peritonitis, salpingitis and oo-phoritis.

Histologically, focal necrosis is common in the liver.This lesion is thought to be caused by bacterial endo-toxins or the formation of thrombi in the bile ducts.Heterophilic infiltrates are most common in acutelesions. Granuloma formation (without a capsule andconsisting of epithelioid cells and multinucleated gi-ant cells), particularly in the spleen and heart, ismore common in chronic cases. Purulent meningitishas been described in some cases. Endocarditis andcardiac infarct may occur secondary to embolic-thrombotic incidents. Localized lymph follicles maybe described as hyperplastic.

DiagnosisIn acute cases, samples for culture taken from theliver, heart and brain are most diagnostic. Isolationfrom the brain indicates that the strain recovered isactively involved in the disease process. A triggeringfactor might have been necessary to enable the or-ganism to cause septicemia. Special media are neces-sary for culturing L-forms.

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Treatment and ControlAggressive treatment with parenterally adminis-tered antibiotics is the recommended therapy. Pyo-genic streptococci are generally sensitive to penicil-lins, erythromycin, tylosin, spectinomycin,clindamycin and pleuromutilin. Enterococci havevarying antimicrobial sensitivities. Chronic joint andtendon sheath infections are difficult to resolve andmay require a combination of surgery, joint lavageand prolonged antibiotic therapy. Joint lavage ap-pears to be more successful in birds than in mam-mals because iatrogenic secondary infections are lesslikely. Streptococci in synovial membranes are fre-quently in their L- or protoplastic form. Treatment inthese cases consists of ampicillin and erythromycinor enrofloxacin (Figure 33.10).

Mycobacterium (M.)

Colony morphology of pathogenic mycobacteriummay be smooth or rough and change through succes-sive in vitro subcultures. Most strains are nonphoto-chromogenic and may become yellow with age. Somestrains are scotochromogenic and have bright yellowpigments.

All bird species that have been experimentally ex-posed have been found to be susceptible to M. avium.Lesions are typified by large numbers of bacteria ininfected tissues. This is in contrast to M. tuberculo-sis, which is typically found in relatively small num-bers in infected tissue. M. avium is highly resistantto environmental extremes and can survive in thecage or aviary environment for periods ranging frommonths to years. Shedding from an infected hostoccurs primarily in the feces and urine, causing con-tamination of the soil or water supplies within theaviary. Mycobacterium has been found to remaininfectious in soil for up to seven years. For disinfec-tion, only compounds tested against mycobacteriumare recommended.

M. avium and M. intracellulare: DNA cleavagetechniques (restriction fragment length polymor-phism and pulsed-field gel electrophoresis) haveshown that M. avium consists of three clusters on thesubspecies level as follows:62

M. avium subsp. avium: This subspecies is ubiqui-tous in the environment and is the agent most com-monly associated with avian mycobacteriosis. Theorganism also has a widely documented mammalianhost range including cattle, sheep, goats, pigs, cats,kangaroos and humans. In humans, adults typicallydevelop respiratory infections, children usually de-velop submandibular adenopathies, and dissemi-nated infections are common in patients with immu-nosuppressive diseases (eg, AIDS). Strainsexperimentally caused paratuberculosis in cattle andtuberculosis in fowl (Table 33.5).

M. avium subsp. paratuberculosis: This subspecies ofM. avium requires mycobactin for in vitro cultureand has not been isolated from the environment. Thissubspecies is considered to cause paratuberculosis inruminants and has been implicated as a cause ofCrohn’s disease in humans.

M. avium subsp. silvaticum: Like M. avium subsp.paratuberculosis, these strains also require mycobac-tin for primary cultivation and have not been recov-ered from the environment. Most strains have been

FIG 33.10 White streaking is evident in the pectoral musculatureof an Amazon parrot that was being treated with IM enrofloxacin.

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isolated from Wood Pigeons and free-ranging rumi-nants. The agent causes paratuberculosis in mam-mals and mycobacteriosis as well as paratubercu-losis in birds.

M. intracellulare is designated as a distinct speciesand is considered less pathogenic to birds than M.avium (whether justified or not). Morphologic, bio-chemical and serologic differentiation between M.avium and M. intracellulare are relatively difficult.These two species are routinely grouped togetherinto the M. avium-intracellulare (MAI) complex. MAIcomplex strains are serologically distinct and havebeen divided into serovars.64 M. avium is divided intoserovars 1 to 11; M. intracellulare into three subspe-cies (subspecies 1: serovar 12 to 17, 19 to 28; subspe-cies 2: serovar 7; subspecies 3: serovar 18). Serovar 1is most prevalent and pathogenic in the UnitedStates, while serovar 2 is most common in Europe. Todate, serovar 3 has mainly been isolated in Europe.

Serovar 8 has been isolated worldwide and is prob-ably the most frequent serovar reported. Birds livingin aquatic environments are particularly susceptibleto infections, which can be subclinical. Recently, se-rovars 25 and 27 have been isolated from sick birds.In addition, M. avium strains have been recoveredthat do not belong to serovars 1 to 28. These newlyisolated strains vary serologically, have a broad hostspectrum and are considered as virulent as serovar 2.38

TransmissionAvian mycobacteriosis primarily involves the alimen-tary tract. Transmission occurs mainly through con-taminated feces, although aerogenic routes of trans-mission are possible. Arthropods can serve asmechanical vectors of M. intracellulare and M. aviumsubsp. avium. Egg transmission can occur but isepornitically unimportant because M. avium bacter-emia causes an immediate cessation of egg produc-tion. Mycobacteria may persist in contaminated soil,litter and, less frequently, feed. Birds of prey can besecondarily infected while consuming infectedquarry. The incidence of mycobacteriosis in free-ranging birds is estimated to be less than 1%.59

PathogenesisThe main portal of entrance in birds is the intestinaltract, which typically results in a visceral infection.Initial colonization occurs in the intestinal wall. Sub-clinical bacteremia occurs early with subsequentspread to the liver through the portal circulationduring the infectious process (relatively low numbersof organisms in the blood). The lack of lymph nodesallows unabated hematogenous spread within thehost. The lungs can be secondarily infected duringbacteremia. Avian mycobacteria are removed fromthe endothelium of the vessels by reticuloendothelialcells, mainly in the liver, spleen and bone marrow.Locally, avian mycobacteria induce cellular reactionsgoverned by the cell-mediated immune system. Incontrast to this typical M. avium infection, Columbi-formes, Anseriformes and some weaver finches of thegenus Textor develop lesions only within the lungs(Figure 33.11). An acute bacteremia is frequentlyobserved in cranes (Gruiformes), the Hermit Ibis,Columbiformes and some Passeriformes. Tuberclesthat form at the site of infection in the intestinal wallcommonly remain open to the intestinal lumen. Thisallows for constant shedding of M. avium into thefeces (open infection). In birds, three different typesof lesions can be recognized although the pathogene-sis has not been clarified: 1) classical form with tu-bercules in many organs; 2) paratuberculous formwith typical lesions in the intestinal tract (prone to

TABLE 33.5 Zoonotic Potential of Bacteria From Companion Birds

Bacteria Zoonotic Potential

Actinobacillus None reported

Alcaligenes None reported

Bordetella None reported

Campylobacter Undetermined, possibleC. laridis – diarrhea in children

Clostridium Negligible

E. coli PossiblePrevention – good hygiene

Erysipelothrix Persistent dermatitisAvoid contact with infected birds

Haemophilus None reported

Listeria Conjunctivitis when infected from birds

Klebsiella Theoretically possibleNone reportedHumans – Friedländers pneumonia

Megabacterium Avian-specific

Mycobacterium PossibleImmunosuppressed humans

Pasteurella Rare human cases

Pseudomonas PossiblePrevention – good hygiene

Salmonella Negligible (see text)

Staphylococcus aureus NegligibleAvian-adapted strains

Streptococcus/Enterococcus

NegligibleBirds may be infected by humans

Francisella tularensis Possible/unlikely from birds

Vibrio Mild enteritis

Yersiniapseudotuberculosis

High potentialTransmission documentedHumans – difficult to treat

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develop this form of myobacteriosis are Amazona,Pionus, Brotogeris, Psittacula species and theHorned Parakeet); 3) non-tuberculous form, whichmay be difficult to recognize at necropsy (many Psit-taciformes).

Clinical DiseaseIn some bird species the clinical course is atypical,and acid-fast rods have been detected more or lessaccidentally. This is particularly the case with smallPasseriformes, especially the Hooded Siskin.19 Clini-cal signs associated with mycobacteriosis are highlyvariable. Adult birds usually develop a chronic wast-ing disease associated with a good appetite, recurrentdiarrhea, polyuria, anemia and dull plumage. Imma-ture individuals frequently develop subclinical condi-tions. Intermittent switching lameness may occur asa result of painful lesions in the bone marrow. Arthri-tis, mainly of the carpometacarpal and the elbowjoints or tubercle formation of the muscles of thethigh or shank can be seen occasionally. These clini-cal changes are particularly common in Falconifor-mes and Accipitriformes. Skin over the affected jointis often thickened and ulcerated. Tubercle formationin the skin is rare, but when it is present, pinpoint topigeon egg-sized nodules filled with yellow fibrinousmaterial may be noted. Granulomas may be seenwithin the conjunctival sac, at the angle of the beak,around the external auditory canal and in the oro-pharynx. Mycobacteriosis should be suspected whentumor-like lesions recur after surgery. Greater Rheafrequently develop granulomas in the upper phar-

ynx. In the Goshawk, loss of balance, convulsions andnecrosis of the base of the tongue have been ob-served.43 Clinical signs associated with colonizationof the lung are rare. However, the peafowl may de-velop respiratory sounds caused by granuloma for-mation within the trachea.

PathologyThe pathology associated with M. avium infectionsvaries widely, probably based on the species of birdinfected and the serovar of the bacterium. Specificrelationships between avian hosts and individual se-rovars have not been defined. The presence of miliaryto greater-than-pea-sized nodules in the wall of theintestinal tract and in the liver, spleen and bonemarrow are characteristic of M. avium infections.These typical lesions have been described in Falconi-formes, Accipitriformes, Strigiformes, Phasianifor-mes, Charadriiformes, Ciconiiformes, Cuculiformes,Piciformes and Ralliformes. Granuloma formationcan occur in any organ but is generally localized tothe intestinal tract and reticuloendothelial organs.The nodules are frequently necrotic in the center andin chronic cases may be calcified. In contrast, Colum-biformes, Anatiformes, Passeriformes and most ofthe Psittaciformes do not form typical granulomas.Acid-fast rods are found distributed throughout theparenchyma of infected organs. An infected liver orspleen may be only swollen or may show necrotic focior even general induration. In pigeons, liver lesionsmay resemble Trichomonas abscesses. In pelicans,greasy tumor-like swellings like those seen in leuk-osis may be observed. The lungs, particularly ofgeese, weaver finches (genera Queleopsis, Quelea andEuplectes) and some Amazona spp., develop necrotiz-ing or ulcerating lesions. Paratuberculous lesions arecharacterized by the occurrence of clubbed villa con-taining acid-fast rods in the intestinal mucosa. Le-sions may also occur in glands of Lieberkühn, withcharacteristic proliferation of their epithelial cells.

Histopathologic identification of foci of single or con-fluent epithelioid cells in affected organs is sugges-tive of an M. avium infection. Parenchymal lesionsgenerally consist of epithelioid cells or multinu-cleated giant cells (mostly the foreign body type, onlyrarely the Langhans type) and occasionally containlymphocytes and plasma cells. Acid-fast rods in vary-ing quantities can be demonstrated in the affectedepithelioid or multinucleated giant cells. Acid-fastrods may also be noted in tissues in the absence ofcellular reactions. Some infected birds will have cell-free acid-fast rods in the proventriculus or jejunalvilli without an inflammatory response. It has been

FIG 33.11 In Psittaciformes, mycobacteriotic lesions are generallynot limited to the intestinal tract. In Columbiformes and someother species, atypical granulomas may form in the lungs. Myco-bacterium avium was recovered from the lungs of this pigeon thatwas presented for severe emaciation and severe dyspnea. Radio-graphs indicated soft tissue masses in the lungs. Abnormal clinicalpathology lesions included WBC=54,000 and PCV=19.

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postulated that the acid-fast rods may actually becontained within lymphatic vessels in the villi. M.avium infections frequently induce depletion of lym-phocytes in the spleen (particularly the white pulp)and a proliferation of macrophage or reticular celltypes in the same tissue. Depletion of the spleniclymphocytes and lymph follicles may induce an im-munosuppression.

DiagnosisThe demonstration of acid-fast rods in tissues or oncytologic preparations is suggestive of mycobacte-riosis. False-negative staining can occur by not ob-taining an adequate sample. The demonstration ofacid-fast rods in the feces has been suggested as auseful diagnostic tool in subclinical birds. Mucuspresent in the feces can interfere with test results,and samples should be processed with one of thesputum solvents used in human medicine beforestaining. The most consistent results can be obtainedby centrifuging the feces and then spreading thesurface of the pellet on a slide for staining. This testis relatively insensitive and requires the presence ofapproximately 104 bacteria/g of feces to be positive.The clinician must differentiate between pathogenicand nonpathogenic strains of mycobacteria, both ofwhich may be present in the feces. In general, non-pathogenic strains are wider and are not granular.Demonstrating acid-fast organisms in the stool is notdiagnostic for a mycobacterial-induced disease.

Culture is required to make a distinct diagnosis.Some strains of M. avium-intracellulare require my-cobactin and will not grow on egg medium. M. aviumsubsp. paratuberculosis and subsp. silvaticum can beseparated by responses to six parameters: subsp.paratuberculosis has a mycobactin requirement,grows on egg medium, tolerates cycloserine (50µg/ml), is stimulated by pyruvate but not by pH 5.5,and has no alkaline phosphatase. The subsp. silva-ticum has the opposite characteristics.62

Unfortunately, most of the mycobacterial strainsfrom Psittaciformes have not been cultured. The fu-ture availability of species-specific antibodies willhelp in delineating infections. Endoscopy (with biop-sies) can be used for diagnosis in cases of advancedclassical tuberculosis. Radiographs may indicategranulomas in respiratory tissues in some cases.Biopsy is required to differentiate between mycobac-terial and fungal granulomas, which radiographi-cally appear similar.

Several indirect tests have been discussed for diag-nosing Mycobacterium. The tuberculin test (aller-genic test) and the slide agglutination test (serologictest) have both been used in birds with some success.The tuberculin test is frequently associated withfalse-negative results, particularly in early and latestages of the disease and is no longer recommended.The slide agglutination test requires fresh plasma orserum and is evaluated against a bank of antigens forthe different serovars; there are cross-reactions be-tween the different serovars. Unfortunately, only se-rovar 2 antigen is commercially available. To esti-mate the probability of an acute disease process,serotitration (using the Gruber-Widal scheme) is pos-sible. Only titers greater than 1:64 are consideredpositive. Psittaciformes may exhibit a cyclic reduc-tion in titer and mycobacterial excretion, which maylead to an incorrect suspicion that natural healing ora successful therapy has occurred. An ELISA systemhas been tested to distinguish between M. aviumserovars but has been hampered by a high degree ofcross-reactivity.

Treatment and ControlSeveral treatment modalities have been discussedfor birds with M. avium infections. However, treatinginfected birds is not recommended because:

All M. avium isolates that have been tested aretotally resistant to the antituberculous drugs rou-tinely used in humans. Recent information re-vealed that ethambutol, while ineffective, doeschange the cellular wall of M. avium in a mannerthat allows other tuberculostatics to enter theorganism.21 However, successful therapy is thendependent on pharmacokinetic conditions and re-quires a combination of drugs to be available at thesame time, at the correct concentration and at thecorrect anatomic location. The pharmacokineticdata necessary to ensure that these parametersare met are not available for a single avian species.M. avium infections are considered to be “open,”allowing infected birds to continuously shed largenumbers of organisms into the environment.There is potential danger to man, and there is noappropriate method of treatment for infected hu-mans.

Birds that are definitively diagnosed (biopsy of af-fected tissue with histopathology and culture) withM. avium or M. intracellulare infection should beeuthanatized. Contact birds should be removed fromthe contaminated area, quarantined for two yearsand tested every six to 12 weeks to determine if they

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are reacting. Birds that remain negative (also notshedding the agent with the feces) and are in goodphysical condition following the quarantine proce-dure can be considered free of the disease. There arecurrently no absolute means of control. The chancesof introducing M. avium-positive birds to the flockcan be reduced by performing serologic or repeatedfecal examinations of all new additions during thequarantine period.

The transmission of M. avium to humans is possible.However, transmission is probably dependent on in-herent resistance, the immune status of the personin question, the frequency of exposure and the num-ber of bacteria per exposure.

M. tuberculosis: M. tuberculosis lesions in Psittaci-formes are possible but are extremely rare. Whenpresent, they are generally characterized by the for-mation of benign localized granulomas of the dermis,frequently around the cere or nares as well as theretroorbital tissue.63 Birds affected are usually petswith very close human contact and, as such, serve assentinels for patent tuberculosis in the owners. Theaffected dermis looks granulomatous and may evenulcerate. The swelling of the retrobulbar tissuecauses a protrusion of the eye (exophthalmos). Diag-nosis can be made by histology or culture of biopsies.Infected birds should be euthanatized.

M. bovis: M. bovis was associated with a generalizedinfection in an Amazon parrot. This animal developeda nontubercular lesion similar to those seen in Psit-taciformes infected with M. avium intracellulare. Thestrain in question was sensitive to all common tuber-culostatic drugs.

Erysipelothrix (E.)

Erysipelothrix rhusiopathiae can induce an acute-to-subacute septicemic disease. Infections are mostcommonly discussed in ducks and geese but can occa-sionally occur in other avian species including Psit-taciformes.55,32 The eleven serotypes of E. rhusiopa-thiae are ubiquitous in the environment and canpropagate outside the host. Survivability in moistsoil and in the water of shallow lakes and ponds, evensalt and seawater, is particularly high. Infections inbirds occur most frequently in the late fall, winterand early spring (northern hemisphere). Rodents,pigs and raw fish have all been implicated as reser-voirs for the bacterium.

PathogenesisE. rhusiopathiae infections are most common in wa-terfowl and fish-eating birds during cold weatherwhen food is scarce and energy requirements arehigh. Concomitant infections and inadequate hy-giene seem to be precipitating factors of natural dis-eases. Most affected birds die during the bacteremicphase of an infection. Those birds that survive theacute disease frequently have secondary dermatitisand arthritis caused by hypersensitivity reactions.

Clinical Disease and PathologyE. rhusiopathiae usually causes peracute death. Ifclinical signs occur, they may include lethargy, weak-ness, anorexia and hyperemia or bruising of thefeatherless, nonpigmented skin. Greenish discoloreddroppings, dyspnea and nasal discharge have beenreported in some cases. In the Marabou Stork, infec-tions have been characterized by inflammation andnecrosis of the cutaneous adnexa of the neck.

Petechiae in the subcutis, musculature and intesti-nal mucosa are common gross lesions in diseasedbirds. The liver and spleen are friable and discolored(red to black). Histologically, these organs are degen-erated and necrotic. Chronic E. rhusiopathiae casesare rare but have been reported in geese and turkeys.Clinical changes associated with this form of diseaseinclude thickened, leather-like skin, serofibrinousarthritis or valvular endocarditis. Histologic changesin these tissues include thrombi and degeneration ofvascular walls.

DiagnosisDiagnosis is confirmed by isolating E. rhusiopathiae.The best samples for isolation (if the tissues arefresh) are liver or spleen. In severely autolytic cases,bone marrow samples may be the most diagnostic. Asin most bacterial diseases, cell-mediated immunity ismore important in resolving infections than the de-velopment of humoral antibodies. Thus, serologicmethods of diagnosis are of little value.

E. rhusiopathiae adjuvanted bacterins have beenused to control flock outbreaks; however, vaccinationmay sensitize the birds and potentiate chronic dis-ease. Flock control can best be implemented throughsound aviary hygiene and rodent control.

Listeria (L.)

Listeria monocytogenes causes β-hemolysis on bloodagar. The motility of listeria is dependent on theambient temperature to which it is exposed. Listeria

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spp. may infect a number of avianspecies, including Psittaciformes.32

Canaries appear to be more suscepti-ble to infections than other birds.

L. monocytogenes is a ubiquitous or-ganism that is frequently found inareas. The bacteria is environmen-tally stable and can propagate out-side the host.56

PathogenesisThe role of L. monocytogenes as aprimary pathogen is controversial;however, there is no question thatingested bacteria can lead to a latentor abortive infection. Acute disease ischaracterized by bacteremia pro-gressing to death within one to twodays. The subacute and chronicforms of the disease involve reactionsof the cell-mediated immune system.Intracellular bacteria like L. monocy-togenes typically induce cell-medi-ated immunity.

Clinical Disease and PathologyClinical disease is usually associated with sporadicdeaths in a collection. Epornitics can develop in ca-naries and related birds that are maintained indense populations. Chronic infections can induce le-sions in the heart, liver and, rarely, the brain. Ifclinical signs are noted, they are generally associatedwith CNS signs and include blindness, torticollis,tremor, stupor and paresis or paralysis (Figure33.12).41 Subacute-to-chronic cases usually cause asevere monocytosis (10 to 12 times normal).

The presence of serofibrinous pericarditis and myo-cardial necrosis is considered suggestive of Listeria.There are usually no gross lesions evident in thebrain. There may be no lesions in birds that dieacutely, or there can be a few petechiae present.

Histologically, infections are characterized by degen-erative lesions, without a cellular response, in theheart and liver. Brain tissue is usually normal, evenin cases in which CNS signs are present and theorganism can be recovered from the cerebrum.

DiagnosisA confirmed diagnosis requires the isolation of L.monocytogenes from affected tissues. Appropriatetransport media are necessary for proper shipment of

samples. Listeria isolates must be speciated, becauseL. ivanovii, L. innocua and L. seeligeri are commonlyrecovered from birds.8 There is little information onthe pathogenicity of these Listeria spp. although L.innocua is considered apathogenic.37 Latent infec-tions limit the diagnostic value of serologic tests(slide agglutination).

Clostridium (Cl.)

The genus Clostridium includes a group of ubiqui-t o us bac te r ia t hat ar e co ns id e re d t o beautochthonous flora in raptors and in birds with welldeveloped ceca, including Phasianiformes (gallina-ceous birds) and Anseriformes. In birds in which thececum is small or absent, clostridium is rarely iso-lated from the intestinal tract and when it is, it isoften considered to be transitory.

PathogenesisClostridium spp. produce more potent toxins thanany other bacterial genus. The pathogenesis of Cl.spp. toxin-induced damage in a bird remains poorlyunderstood except for Cl. botulinum. This Cl. sp.principally causes an alimentary intoxication. Theability of clostridia to colonize the intestines appearsto depend on reduced gastrointestinal motility. Peri-staltic abnormalities can occur as a result of enteri-tis, low levels of dietary fiber, administration of some

FIG 33.12 Encephalitis caused by several bacterial pathogens including E. coli, Listeria,Salmonella, Staphylococcus and Klebsiella spp. can cause neurologic signs characterizedby torticollis, tremor, ataxia, depression, paresis or paralysis.

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medications, or during some viral infections (particu-larly reovirus). Experimental reproduction of diseaseby using a culture alone is usually not possible, andclostridial organisms are considered to be opportun-istic pathogens. Following colonization, pathogenicclostridia produce exotoxins, which then induce clini-cal lesions or death.

It is best to discuss clostridial infections by groupingthem under clinical signs because a clostridial spe-cies can cause differing clinical signs, and variousclostridial species can cause similar-appearing dis-eases.

Necrotic or Ulcerative EnteritisClostridia-induced enteritis can occur in many avianspecies. Flock outbreaks are most commonly associ-ated with Phasianiformes, especially those withinthe subfamilies Tetraoninae (grouse) and Odonto-phorinae (New World quail) or captive and free-rang-ing lorikeets.44 Ulcerative gastritis, not enteritis, isthe most common form of clostridial infection re-ported in the ostrich.60 Clostridial enteritis in gamebirds (Tetraoninae) is usually associated with Cl.perfringens type A. On rare occasions, types B, C orD may be the etiologic agent. Cl. perfringens type Eis vary rare in Phasianiformes. Ulcerative enteritisin the Bobwhite Quail is usually caused by Cl.colinum (species incertae sedis). This organism isalso thought to cause necrotic enteritis in the otherOdontophorinae, grouse, chicken, turkey and domes-ticated pigeon (Köhler, personal communication).

Necrotic enteritis usually occurs in young birds afterthe second post-hatching week. Adult birds are moreresistant. In the acute form of the disease, clinicalchanges include diarrhea (with or without blood) andpolydipsia, followed by death within a few hours.Birds with chronic lesions exhibit retarded growthand weight loss before dying.

Pathologic changes include diffuse or focal hypere-mia of the mucosa, which develops into necrotic areasor ulcers. These lesions are most common in theupper jejunum. Lesions start as pinpoint foci andprogress to include a necrotic center with a wall anda reddish halo. Ulcers may coalesce and perforate theintestinal wall. Swelling and necrosis of a grayishliver, spleen and kidney are common.

Identification of characteristic lesions and isolationof the organism are confirmatory. If Cl. perfringens isthe etiologic agent, a diagnosis can be achieved bydemonstrating toxins in the serum, intestinal con-tents and liver homogenates (sterilized by filtration).

The differential diagnosis includes salmonellosis, en-terotoxic E. coli and drug overdoses. Newcastle dis-ease virus can induce ulcers called “boutons” thatresemble those induced by Clostridium.

Gangrenous DermatitisGangrenous dermatitis can be caused by Cl. perfrin-gens type A, Cl. septicum, or Cl. novyi. These organ-isms can directly colonize damaged skin. Microscopicepithelial lesions caused by abrasions, avipoxvirus orstaphylococci can become secondarily infected withClostridium spp. The patient’s immune status mayalso play a role in the overall pathogenesis.

The sudden occurrence of regional feather loss witha blue-red or almost black skin discoloration is acharacteristic lesion. Affected skin may also be ede-matous and painful as a result of gas accumulationin the tissue. Sick animals typically develop toxemiaand die within 24 hours. With screamers (genusChauna), their corneous-lined bony wing spurs cancause prick-like skin injuries predisposing them toclostridial diseases.

The occurrence of emphysema, edema and hemor-rhages (with or without necrosis) in the subcutis,skeletal musculature and myocardium are charac-teristic necropsy findings. A confirmed diagnosis re-quires isolation of Cl. spp. from affected tissues.Aeromonas hydrophila, s ta p hy lo co c c i andavipoxvirus can induce pathologic changes similar tothose caused by Cl. spp. Rapid production and sys-temic release of toxins usually prevents successfultherapy.

Botulism (syn. Limberneck)

Cl. botulinum neurotoxins are typically ingested incontaminated foods. Rarely, clinical disease may re-sult from primary colonization of the alimentarytract. Cl. botulinum has been found to produce sixthermolabile exotoxins (designated A to F). Types Aand C are predominantly involved in inducingpathologic changes (occasionally also type E). Highconcentrations of clostridium toxins are common indecaying meat and vegetation. Fly larvae (maggots)that feed on decaying material are resistant to thetoxins but can serve as a source of intoxication forthose species that eat maggots. With a few logicalexceptions, most birds are probably susceptible to Cl.botulinum toxins. Free-ranging waterfowl are par-ticularly susceptible, and enzootic intoxications arecommon following periods of drought or flooding.Vultures seem to be resistant to the toxins (by a still

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unknown mechanism), and some raptors (that eatcarrion) have a reduced susceptibility.

Foods contaminated with Cl. botulinum toxins haveno particular change in taste or smell and are thusdifficult to detect. Toxins enter the body through theintestinal wall, move to the ends of the autonomicand somatic efferent nerves and then ascend into thespinal cord. Once in the spinal cord, toxins selectivelyand irreversibly bind to the neuromuscular junctionsand block the production of acetylcholine. Death isdue to respiratory paralysis. Toxins also damage vas-cular endothelium, resulting in edema and petechia-tion.

Flaccid paralysis of the skeletal musculature (includ-ing the tongue) is the characteristic clinical change.Bulbar paralysis, feather loss and diarrhea may benoted in some birds. Birds with substantial clinicalsigns usually die, although a few can spontaneouslyrecover. Recovery is more likely with type A ratherthan type C toxin. Petechial hemorrhage of the cere-bellum and focal necrosis and hemorrhage of thecentral lobe of the cerebrum are indicative of Cl.botulinum, but there are no pathognomonic lesions.

Confirming a diagnosis requires using mouse animalmodels to demonstrate the presence of toxins in se-rum, filtered liver or kidney from an affected animal.Feed or water (sewage, mud) extracts from a pondalso provide diagnostic samples. Cl. botulinum tox-ins are heat-sensitive and degrade at room tempera-ture. Materials to be tested should be preserved bydeep-freezing (-20°C).

Intoxication with some algae, eg, red tide (see Chap-ter 46), may cause clinical signs similar to thosecaused by Cl. botulinum. Affected birds usually haveaccess to muddy, drying bodies of water. Aeromonashydrophila can cause the acute death of large num-bers of waterfowl that consume contaminated water.A rapid death, typically in the summer, is charac-teristic, but some infected birds can develop signsthat mimic those of Cl. sp. toxin ingestion. A. hydro-phila and Cl. botulinum may both cause epornitics ofacute death in connection with contaminated water.

Flock problems can be prevented by reducing contactwith decaying foods, removing cadavers, providingtoxin-free feed (especially for insect eaters) and regu-lating the water level and temperature in waterfowlcollections (see Chapter 46). A commercial type Cantitoxin is available for mink and has proven to beeffective in birds. One-half of the dose recommendedfor mink should be used in birds.

Tetanus

A few cases of Cl. tetani intoxication in birds havebeen reported in older literature. There have been nocases of tetanus reported in birds using more confir-matory diagnostic tests. Generally, birds are consid-ered to be highly resistant to Cl. tetani; cases re-ported in older literature may have been incorrectlydiagnosed.

Other Gram-positive Rods

Bacillus spp., Corynebacterium spp., Streptomycesspp. and Lactobacillus spp. are commonly recoveredfrom avian-derived samples. Because these organ-isms are frequently isolated from clinically normalbirds, they are considered to be components of theautochthonous flora. Megabacterium is considered tobe a pathogenic organism, although little informa-tion is currently available on its involvement in aviandisease. Bacillus spp. isolated from birds are difficultto differentiate, and most have not been describedtaxonomically. Bacillus anthracis has not been asso-ciated with clinical disease in birds, presumably be-cause their high body temperature inhibits the pro-duction of the pathogenic toxins. Vultures, and to alesser extent raptors, are known to be mechanicalvectors.

None of the Corynebacterium (Co.) spp. that havebeen isolated from birds have been found to be patho-genic. Ostriches have been reported to have concomi-tant Co. pyogenes and Sc. group C infections.32 Anti-bodies to Corynebacterium spp. and Mycobacteriumavium-intracellulare can cross-react, making differ-entiation between these organisms difficult.

Streptomyces spp. can occasionally be isolated fromthe avian respiratory system. The pathogenicity ofthe organism is questionable. Some reports describenocardia in birds. These cases were described basedon bacterial morphology and not on analysis of wallcomponents, which is necessary to confirm nocardiain infected tissues.

Lactobacillus spp. can be identified on the mucosa ofthe intestinal, respiratory and reproductive tracts ofmany avian species. In birds that do not possessEnterobacteriaceae as a normal component of the gutflora, lactobacillus seems to play an important role ininhibiting colonization of Enterobacteriaceae (al-though probably not in many species of grouse). Sup-plementing with lactobacillus has been discussed asa method of inducing a natural competitive inhibition

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TABLE 33.6 Survey of Clinically Important Bacteria

Bacteria Characteristics Incubation Transmission Disinfectants/Stability

Alcaligenes/Bordetella

Motile0.3-0.5 x 1-2 µm

Turkeys – 5-7 daysOthers – unknown

Alc. ingestionShed in fecesEgg transmissionBord. respiratory tract, fecesEgg transmission

Resistant to dryingEnvironmentally stable(Particularly low temps)

Campylobacter Gram-negativeMotile rod0.2-0.5 x 1.5-5 µm

5 to 15 days IngestionFeces

Survives 1 week out of hostMost disinfectants effective

Clostridium Gram-negativeAnaerobicSpore-forming rod

Experimental – hrs to 3 daysNatural – unknown

IngestionWound infection

Resistant in environmentSpores – survive yearsMost disinfectants ineffectiveAutoclaving/flaming effective

Erysipelothrix Gram-positiveNonmotile rods0.2-0.4 x 1-2.5 µm

Turkeys, ducks – 1.8 daysOther birds – unknown

IngestionEgg transmission (stork)

Most disinfectants effective

E. coli Gram-negative0.5 x 3 µmMotile or nonmotile rod

Experimental – 24 to 48 hrs Ingestion – mainlyAerogenic – dustEgg transmission(normal & L-forms)

Most disinfectants effective

Haemophilus Gram-negative0.3-0.6 x 1-3 µmCoccoid-to-pleomorphic rods

H. paragallinarum1-5 days

Respiratory tractAsymptomatic carriers

Survives a few daysMost disinfectants effective

Listeria Gram-positive0.4 x 0.5-2 µmMotile rod

Unknown IngestionCommon in aquatic environmentsReptiles, amphibians, snails natural reservoirs

Most disinfectants effective

Mycobacterium Gram-positiveAcid-fastGranulated short-to-long rods

Weeks to yearsExposure and immune systemdictate

Feces, urineAerogenic possible (rare)Arthropods-mechanical vectors

Persists in contaminated soil or litter for years

Pasteurella Gram-negativeNonmotileOvoid-to-coccoid rod

Vary with speciesCat bite – 6-48 hrs

Upper respiratory tractFecal shedding rareSee text

Not stable to stabledepending on conditionsMost disinfectants effective

PseudomonasAeromonas

Gram-negative1-3 x 0.3-0.6 µm

Specifics unknownPseud — few hrsAero — 1-3 days

IngestionProliferates in H20Secondary in open wounds

Pseudo: resistant to most disinfectants – steam, boiling H20 effectiveAero: most disinfectants effective

Salmonella Gram-negative0.5 x 3 µmMotile, rarely nonmotilerod

Varies with typeAcute 3-5 daysEgg — 2 days

IngestionEgg transmissionNormal and L-forms

Dried feces stable – 8 months to 2 yearsWater stable – 3 weeksMost disinfectants effective>60°C kills most strains

Staphylococcus Gram-positive0.8 x 1.0 µmNonmotile Spherical coccoid

UnknownFew hrs to few monthsLatent infections

Vertical, horizontalNormal & L-formsChronic carriers

Environmentally stableMost disinfectants ineffective

StreptococcusEnterococcus

Gram-positive <2 µmCoccoid-to-ovoid pairs or chains

Mammals – days to weeksBirds – unknown

Horizontal, verticalShed in fecesAerogenicPercutaneous (skin lesion)

Probably no growth in environmentSc spp – short-livedEc spp – long-lived

Yersinia 0.4 - 0.8 x 0.8 - 1 µmMotile or nonmotileOvoid-to-coccoid rods

Days to 2-3 weeks IngestionCarrier birds & rodentsDirect contactFecal contaminated food orwater

Most disinfectants effective

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of gram-negative and other pathogenic bacteria. How-ever, there are strong indications that many groups ofbirds have specific lactobacilli that can effectively colo-nize the gut. Strains derived from soured milk do notcolonize the avian gut and must be given daily for twoto four weeks in order to lower the gastrointestinaltract pH. This drop in pH will favor the colonization ofautochthonous microorganisms. Inhibitory expulsionitself takes from four to six weeks, provided no serioustriggering factors interfere.23

Isolation of megabacteria is difficult, and biochemi-cal descriptions that would allow appropriate taxo-nomic classification have not been performed. Thisorganism has a unique morphology and is a large (1x 90 µm) gram-positive rod.13 Successful culture re-quires the use of Merck’s MRS medium; however, notall megabacterial strains have been found to grow onthis medium. The colonies are rough and measure 3to 4 millimeters in diameter with a dented margin.Development requires 48 hours in a moist chamber.Subcultures are progressively more difficult and theorganism may stop growing in successive passages.28

TABLE 33.7 Bacterial Control and Therapeutics

Bacteria Treatment/Control

Actinobacillus Tetracyclines/chloramphenicol See text

Aeromonas Most antibioticsSee text

Alcaligenes/Bordetella Antibiotic resistance commonRx based on sensitivities

Borrelia Tylosin/SpectinomycinControl ticksStrain-specific vaccines

Campylobacter Erythromycin/tetracyclinesStreptomycin, non-psittacinesFurane derivatives in non-waterfowl(See text)

Clostridium perfringens Clindamycin/spiramycinLaxatives – Remove unabsorbed toxinsWound irrigationControl – Vaccination (toxoid) Zinc bacitracin (200 ppm) (Bobwhite Quail in food) Prevent skin wounds

Clostridium botulinum Toxoid vaccine, antitoxinLaxatives – remove unabsorbed toxinsGuanidine – (15 to 30 mg/kg) May bind neurotoxinPrevent food contaminationActivated charcoalSee text

Cytophaga Parenteral antibioticsTreat soon after hatchingBacterins provide sero-specific protection

Escherichia coli Rx based on sensitivitySee text

Erysipelothrix Parenteral penicillin/doxycyclineSurgically remove affected skinHyperimmune serumSee text

Haemophilus Most antibioticsSulfonamides – drug of choiceSinusitis – surgical drainage Flushing Topical vitamin AAsymptomatic carriers Detect by culturing sinusesPolyvalent vaccine – poor efficacy

Bacteria Treatment/Control

Klebsiella Resistant to many antibioticsRx based on sensitivityEnrofloxacin initially

Listeria TetracyclinesCNS signs – poor prognosisHygiene critical

Megabacterium No effective therapyResistant to all tested antibioticsControl – unknownAcidifying water with HCl

Mycobacterium Not recommendedSee text

Pasteurella Parenteral antibioticsSee textControl – Prevent rodents/free-ranging birds Vaccines – poor efficacy

Pseudomonas Resistant to many antibioticsRx based on sensitivityEnrofloxacin initiallySystemic infections usually fatalSee text

Salmonella See text

Staphyloccocus Resistant to many antibioticsSemisynthetic penicillins pending sensitivityBumblefoot – Debride, antibioticsHeparin – prevents fibrin

StreptococcusEnterococcus

Parenteral antibioticsSee textControl – hygieneStimulates minimal immune response

Yersinia See text

Treatment of all bacterial infections should be based on specificantibiotic sensitivity. Supportive care in the form of fluids and enteralfeeding is frequently necessary. Correcting predisposing factors thatcause immunosuppression in the host or allow exposure to an organ-ism are critical control methods. Preventing exposure to rodents,insects and free-ranging birds can reduce bacterial exposure. Hygieneis always important, particularly in neonates, to prevent reinfection.

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FIG 33.13 A group of budgerigars was presented for occasionalmelena and chronic weight loss over a prolonged period. Large (1x 90 µm) gram-positive rods (suggestive of megabacteria) could bedetected in the feces. Radiographs in various affected birds indi-cated a,b) proventricular dilatation and c,d) filling defects andulceration in the proventriculus. At necropsy, the filling defectswere found to be globules of mucin that had a propensity toaccumulate at the isthmus. It should be noted that the presence ofa dilated proventriculus is not diagnostic for neuropathic gastricdilatation (courtesy of Nina Ungerechts).

Morphologically similar strains of megabacteriumthat were considered normal components of thebudgerigar proventricular flora have been de-scribed.53

Some researchers believe that megabacterium is thecausative agent of progressive weight loss (“goinglight syndrome”) in budgerigars. The name “goinglight syndrome” should provisionally be replaced bymegabacteriosis, because weight loss is a clinicalsign of a variety of chronic diseases. Experimentalinfections with pure cultures of megabacterium in-duce disease only in English standard budgerigarsand not in the normal breed.28 These findings suggestthat birds vary in susceptibility to the organism, andother factors are involved in the pathogenesis. Spon-taneous recovery was common in experimental cases.The host spectrum includes canaries34 and relatedfinches, cockatiels, lovebirds, chickens and young(3-week-old) ostriches (Hüchzermeier, unpublished).

Clinically infected birds develop chronic emaciationover a 12- to 18-month period that may or may not

involve intermittent periods of recovery. Severely af-fected birds may pass digested blood in the feces.Contrast radiography typically indicates a sand-glass-like retraction between the proventriculus andventriculus (Figure 33.13). This finding is consideredhighly suggestive of megabacteriosis.31 Megabac-terium is shed in the feces and can be detected bygram-stained samples from severely sick birds.

At necropsy, a proventriculitis or proventricular ul-cer with or without hemorrhages can be observed.Lesions are most common in the pars intermediagastris. The organisms lie densely together in thenecrotic tissue foci. There is usually little inflamma-tory cellular reaction associated with the organism,which can be seen readily at low magnification fromproventricular scrapings. Impression smears fromthe liver and spleen may be useful in detecting thebacteria, which can be encapsulated in the tissues.There is no treatment because of resistance to allantibiotics commonly used.

TABLE 33.8 Differential Diagnoses of Bacterial Infections

Arthritis or SynovitisStaphyloccoccus Actinobacillus sp.E. coliE. rhusopathiae (ducks and goose)Mycobacterium avium Mycoplasma spp.Pasteurella multocidaSalmonella spp.

CNS SignsListeriosis ChlamydiosisE. coli Klebsiella pneumoniaeListeria monocytogenesSalmonella spp.

DermatitisPseudomonas/Aeromonas spp.Clostridium spp.Staphylococcus spp.

EnteritisE. coliAeromonas sp.Most enteric organismsPseudomonas spp.Salmonella spp.E. rhusiopathiaeChlamydiosisListeria sp.Pasteurella spp.

HepatitisMost bacteria that cause septicemiaCampylobacterPasteurella spp.ChlamydiosisSalmonella spp.

Pseudomonas enteritisClostridium spp.

Respiratory DiseaseAlicalgenesEnterobacteriaceaePasteurella spp.

Cytophaga (duck septicemia)Pasteurella spp.HaemophilusChlamydiosis (eg, psittacines, Columbiformes)Salmonella spp.

SepticemiaE. coliMany bacteriaListeria spp.E. rhusiopathiaePasteurella spp.Salmonella spp.Yersinia pseudotuberculosisPseudomonas/AeromonasMost EnterobacteriacaeStaphylococcus (mimics numerous other infectious agents)Streptococcus/EnterococcusBorrelliosis (high tick areas)

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References and Suggested Reading

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