Haemolytica, Alcaligenes Faecalis) - in General, Bacte-: Acteria

cientific principles of bacteriology are uni-
S versal; however, in application, bacteria can

adapt to their avian hosts, altering the form
and pathogenicity of well known bacterial
species. Avian bacteriology is further complicated by
CHAPTER
33
the fact that bacteria that are as yet taxonomically
undescribed can be isolated from a variety of avian
species. Some of these bacterial strains have been
erroneously classified as taxons (eg, Pasteurella
haemolytica, 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 large
numbers of organisms, repeated exposures, specific
susceptibility or immunosuppression. Some host-
adapted strains may form biovars that are specific to
one avian species (or a few closely related species) as
compared to the dominant species.
Example of Bacterial Taxonomy: BACTERIA

Genus Salmonella
Species S. typhimurium
Subspecies S. typhimurium var copenhagen
Biovar Pigeon strains, chicken strains
Bacterial infections may be primary or secondary.

This differentiation is important for the evaluation of
a disease process. After becoming established, many Helga Gerlach
secondary invaders are able to maintain a disease
process independent of other infectious agents or
predisposing conditions. Laboratory examinations
(biochemical or serologic) are rarely of any help in
differentiating primary from secondary invaders.
The companion bird clinician must determine the
importance of bacterial isolation for a specific bird
species and a specific disease process. Analogous con-
clusions drawn from poultry literature may not be
valid, and experimental infections are frequently not
possible. Some specific points may guide the clinician
in interpreting bacterial culture results (Table 33.1).
950
SECTION FIVE DISEASE ETIOLOGIES
autochthonous flora is considered normal, and only

TABLE 33.1 Guides to Interpretation of Bacterial Culture Results27 the isolation of primary pathogens is really helpful.
Because whole blood has bacteriostatic and bacteri-
Isolation of an organism in an almost pure culture (approxi- cidal properties, blood culture samples must be
mately 80% of the colonies present) may indicate that the
transferred immediately after collection to attenuant
bacteria is a component in the disease process.
containing nutrients and one of the artificial hepari-
Isolating large numbers of bacteria in almost pure culture from
the heart tissue is suggestive of bacteremia, and the isolated noids, for instance Na-polyanetholsulfate. Commer-
agent should be considered part of the disease process. cially available blood culture flasks are also useful.
Isolating a bacteria that is part of the autochthonous flora may
indicate 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 to
determine if the bacteria is a primary or secondary pathogen. Gram-negative Bacteria
Isolating bacteria from parenchyma with pathologic or his-
topathologic lesions suggests that the agent contributed to the
disease process.
of Clinical Significance
Isolating a bacterium without identifying other microorganisms
(virus, chlamydia, other bacteria, fungi, protozoa) suggests that
the agent is a primary pathogen. Finding virus or chlamydia
suggests that the bacterium may be a secondary pathogen. “Intestinal bacteria” are considered to be those spe-
Isolation of bacteria from a bird with fungi and protozoa sug- cies that can colonize the intestinal tract. As a group,
gests that the bacterium is a primary pathogen.
intestinal bacteria can be part of the normal flora or
Obtaining mixed cultures or identifying individuals within a
given flock with different bacterial isolates suggests secondary pathogenic organisms that are not routinely found in
infections are occurring. the GI tract; in some cases, normal flora can become
Isolating small to moderate numbers of bacteria from the liver secondary pathogens. When a bacterium leaves the
or kidney can be “normal,” because birds have hepatic and mucosal surface and penetrates the intestinal wall,
renal portal circulations and lack lymph nodes that filter blood
before it drains into the liver and kidney. Because lymph follicles it then can induce systemic disease, including septi-
are distributed throughout these organs, defense responses cemia and death. The Enterobacteriaceae are consid-
actually occur within the parenchyma and not externally, as in ered the most important avian intestinal pathogens,
mammals. These organs should not be expected to be sterile,
but should be expected to contain autochthonous flora. The but other groups, such as Aeromonas, Pseudomonas,
number of organisms isolated at necropsy depends on the time Alcaligenes, Bordetella spp. and related organisms,
of death and the method of handling the body (eg, storage, as well as Vibrio and Campylobacter, may also colo-
preservation).
nize the gastrointestinal tract.
Enterobacteriaceae
Because the isolation of “unusual” bacteria can be
expected from avian samples, the clinician can en- The members of the Enterobacteriaceae family typi-
hance results by providing the laboratory with a cally grow well on commonly used media. Enterobac-
thorough anamnesis, exact species of the bird in teriaceae are divided into genera based on specific
question, and as far as possible, the names of particu- biochemical and serologic characteristics. Many spe-
lar bacteria that may be suspected in the case. This cies are further divided into biotypes and serotypes.
latter point is especially important if special media In these species, complete identification requires dif-
or environmental conditions are needed for bacterial ferentiation between the O, K and (in motile species)
isolation. In addition, with some organisms, special H antigens. Serologic differentiation between the
transport media and shipping methods (eg, on ice) genera is often difficult since group-specific antigens
may be necessary to preserve the organism. (lipopolysaccharides) can cross-react.
Blood cultures are considered a definitive diagnostic Enterobacteriaceae are able to propagate in the envi-
tool in humans and some mammals. In these species, ronment if they are in the proper conditions. Entero-
samples are, as a rule, taken during a period of fever. bacteriaceae are ubiquitous and considered to be part
A febrile period is difficult to determine in a bird and of the autochthonous intestinal flora in many mam-
is generally considered of minimal importance. In mals, including humans and some species of birds
birds, organs as well as blood are not necessarily (Table 33.2).
sterile, although the number of bacteria is extremely
low. Generally, the isolation of small quantities of
951
CHAPTER 33 BACTERIA
TABLE 33.2 Birds in which Enterobacteriaceae are not normal Pathogenesis

The pathogenesis of E. coli infections in birds is
Psittaciformes (parrots and Gruiformes (cranes)
parakeets) poorly defined. Mammalian strains produce large
Otididae (bustards)
Fringillidae (finches) quantities of exotoxins that cause many of the clini-
Sphenisciformes (penguins)
Ploceidae (weaver finches) cal and pathologic changes associated with infection.
Ciconiiformes (storks, ibises)
Astrildae (waxbills) Except for the presence of enterotoxins, avian E. coli
Tetraoninae (grouse)
Accipitriformes (hawks, strains appear to produce few exotoxins. These en-
Musophagiformes (turacos)
vultures) terotoxins cause diarrhea by inducing hypersecretion
Trochiliformes (humming-
Falconiformes (falcons) birds) of fluids into the intestinal lumen. Endotoxins may
Strigiformes (owls) cause hypersensitivity angiitis followed by septice-
mia and death.
Isolation of Enterobacteriaceae from the respiratory Clinical Disease and Pathology
or reproductive tracts is abnormal. This group of
The clinical signs associated with primary or secon-
bacteria can colonize most avian tissues, where it is
dary infections are thought to be governed by the
frequently considered as a secondary pathogen. In
portal of entry to the avian host.
some cases, Enterobacteriaceae can function as pri-
mary pathogens. Substantial differences exist in the Colisepticemia is characterized by an acute onset of
virulence of the various Enterobacteriaceae and in lethargy, anorexia, ruffled plumage, diarrhea and
the host response to infections. The genera Shigella polyuria. E. coli septicemia usually involves the kid-
and Edwardsiella are normally not cultured from neys, although clinical signs of renal involvement
birds (the latter rarely from pigeons). The genera may or may not be present. CNS involvement is rare.
Enterobacter, Hafnia, Serratia and Proteus are of a Ocular lesions occasionally occur and include exuda-
low pathogenicity. The isolation of Enterobacter ag- tion of fibrin into the anterior eye chamber or uveitis.
glomerans (a plant pathogen) in avian feces can indi- Serofibrinous arthritis can occur as a sequela in some
cate the consumption of seeds that contain more than infected birds. Fibrinous polyserositis, the severity of
106 bacteria/g of food. This bacterium is common in which depends on the chronicity of the infection, may
decaying plant matter; foods containing the bacte- be noted at necropsy. Catarrhal enteritis is common
rium in high numbers should be considered toxic. but nonspecific. The most consistent histologic lesion
Serratia marcescens is increasingly found in large is serofibrinous inflammation with plasma cell infil-
parrots with chronic debilitating diseases. Predispos- tration in the liver and kidneys (Figure 33.1).
ing factors seem to include previous antibiotic treat-
ment and immunosuppression. Localized enteritis caused by E. coli is a result of
enterotoxin production, which induces an increased
Escherichia (E.) secretion of fluids. The resulting diarrhea causes a
substantial loss of electrolytes and proteins and in-
E. coli is the most commonly encountered member of duces dehydration and cachexia. Some strains of E.
this genus; in many avian species it is considered to coli are capable of colonizing and destroying the in-
be a more important pathogen than salmonella (see testinal epithelium. These strains typically induce a
Table 33.6). This genus contains a number of species pseudomembranous or ulcerative enteritis. Clini-
that may be motile or nonmotile, encapsulated or cally infected birds die peracutely or develop nonspe-
nonencapsulated. Classification of the strains of E. cific signs associated with enteritis. Infections with
coli that infect birds has been difficult. The serologic these strains are usually diagnosed on postmortem
and virulence factors used to classify the E. coli examination.
strains that infect humans and other mammals do
not accurately predict which E. coli strains will be Coligranulomatosis (Hjaerre’s disease) is particu-
pathogenic in birds. Although each serovar of E. coli larly common in Phasianiformes including chickens,
includes both virulent and avirulent strains, there turkeys, peafowl, partridges and capercaillie. Mucoid
seems to be a slightly higher frequency of virulent (eg, encapsulated) E. coli strains, mainly of serovars
strains within the serovars 01, 02 and 078. In experi- 08, 09 and 016, are the usual etiologic agents. Coli-
mental transmission studies, all lysine decarboxy- granulomas are thought to occur when other agents
lase-negative E. coli strains have been found to be damage the intestinal mucosa and allow a secondary
virulent in birds. Unfortunately, many of the lysine infection with specific E. coli serovars. It is currently
decarboxylase-positive strains are also virulent.
952
FIG 33.1 A seven-year-old male Amazon parrot was presented for weakness and diarrhea. Abnormal clinical pathology findings included
PCV=22, WBC=33,000, SGOT=476. A Gram’s stain of the excrement revealed 70% gram-negative rods. Radiographs indicated ileus (gaseous
distension of the bowel), a full crop and microhepatia. Dried excrement is visible pericloacally. The dilated bowel loops are displacing the
proventriculus (p) cranially and the ventriculus (v), liver (l) and heart (h) ventrally.
thought that galactans found in the E. coli capsule metastases from infected air sacs. Infections are usu-
stimulate the granulomatous reaction. ally chronic in nature, with untreated birds eventu-
ally dying from salpingoperitonitis. Genital tract in-
Affected birds develop diarrhea, polyuria and chronic fections in males are less common, but when they do
weight loss. Granulomatous dermatitis is occasion- occur they usually result in orchitis and permanent
ally noted. Grayish foci of varying sizes in the liver, sterility.
intestinal subserosa and spleen or kidney are typical
findings at necropsy. These granulomas are distinct Secondary colonization of joints and bone marrow
from those induced by avian tuberculosis because can occur following E. coli septicemia. These lesions
they lack an opening into the intestinal lumen. The are rare, but when the do occur they are most fre-
center of the foci may be mineralized. Histologic quent in nestlings and fledglings. Some of the finch
changes are characterized by multinucleated giant species seem to be particularly susceptible. Bone
cells and a few heterophils around a central necrotic marrow infections appear to be very painful, and
region. Acid-fast staining should be used to rule out affected birds are usually reluctant to move.
mycobacteriosis.
Diagnosis
E. coli can cause a primary rhinitis but is generally a Polyserositis and granuloma formation are lesions
sequela to infections elsewhere in the body. Air sac suggestive of E. coli infections. Specific diagnosis
lesions can be severe and may extend to the perito- requires culturing the organism from infected tis-
neum, causing a fibrinous polyserositis. Except for in sues. Serotyping is of academic importance.
geese, E. coli pneumonia is rare. This is due to the
special anatomy of the avian lung. When pneumonia Treatment
occurs, it is most common in young chicks that have The ability of a selected drug to penetrate target
inhaled a high number of virulent E. coli with con- tissues or granulomas must be considered (see Table
taminated dust. Affected birds are usually dyspneic 33.7). Oral antibiotics may be effective in treating E.
and cyanotic. In contrast to mammals, pneumonia is coli infections limited to the intestinal mucosa, but
not associated with prominent respiratory sounds. parenteral antibiotics are necessary for treating most
E. coli infections. In addition to antibiotics, therapeu-
Hens can develop E. coli infections characterized by tic considerations should also include administration
fibrinous salpingitis or oophoritis originating from of avian lactobacilli in an effort to lower the intestinal
organisms that ascend from the cloaca or by imprint
953
CHAPTER 33 BACTERIA
tract pH and help establish a proper autochthonous spp. that can cause devastating outbreaks. Some
flora. Mammalian strains of lactobacillus can be ef- salmonella strains are host-adapted (eg, S. galli-
fective in changing the intestinal pH but require the narum-pullorum to chickens, S. typhimurium var.
administration of large quantities of product over a copenhagen [in two biovars] to either pigeons [malon-
three- to four-week period. Lactulose may also be ate-negative] or European finches [malonate-positive]).
helpful in lowering the intestinal pH. Providing a
nutritional diet is important in improving gastroin- Transmission
testinal physiology in malnourished birds. Salmonella enters the host principally through the
oral route. Contaminated dust from feces or feathers
may be involved in aerogenic spread in some cases.
Salmonella (S.)
Egg transmission can occur with fully walled and
The genus Salmonella includes approximately 2000 L-form salmonella. It is most common with adapted
species divided into five subgenera. Subgenus I is the strains but is possible with any S. sp. Experimental
most important in birds. Subgenus III (S. arizonae, studies indicate that patent infections in embryos
Arizona hinshawii) has occasionally occur with fewer than ten bacteria. These infected
been reported in birds, particularly
those that are in contact with rep-
tiles. Most strains are motile and
grow 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 used
for further characterization at the re-
search level. Propagation can occur
outside the host if the correct ambi-
ent temperatures and proper nutri-
ents are available.
Most vertebrates can be infected

with some Salmonella spp. However,
the host susceptibility and develop-
ment of carrier states vary widely
among species. Free-ranging birds
can be subclinical carriers and serve
as a reservoir for the aviary. In addi-
tion to free-ranging birds, rats, flies
and other vermin may also serve as
vectors of salmonella. Avian species
without ceca or with involuted ceca
appear to be more susceptible to sal-
monella infections than birds with
fully functioning ceca. Bacteroides
and Spherophorus spp. are consid-
ered autochthonous cecal flora, and
these gram-negative anaerobes may
function as natural antagonists for
Salmonella spp. The incidence of
various S. spp. seems to vary with FIG 33.2 An adult Barn Owl from a zoological collection had a three-year history of
geographic location and the types of intermittent depression and anorexia. The bird was presented with severe right-sided
food consumed, particularly the pro- head tilt and vertical-to-rotatory nystagmus. The external ear canal was hyperemic, and
the tympanic membrane was opaque and edematous. Radiographs indicated a soft tissue
teinaceous component. Imported density in the right tympanic bullae suggesting an internal ear infection. Auditory evoke
birds (and other animals) may serve potentials indicated lesions in the peripheral and central auditory pathways. Klebsiella
as reservoirs for nonindigenous S. sp. and Pseudomonas sp. were recovered from the infratrochlear area and brainstem at
necropsy.
954
chicks then hatch and spread salmonella by direct nella is no exception, and some cases of food poison-
contact throughout a nursery. If an embryo has more ing are linked to this bacterium. Indirect death
than ten bacteria, it usually dies before hatching.47 In through endotoxin contamination of food is rare in
freshly hatched chicks, salmonella often serves as birds; most avian salmonella problems are associ-
the first bacterium to colonize the intestines. This ated with direct infections. Interestingly, both viru-
organism becomes host-adapted during the egg incu- lent and nonvirulent strains of a given Salmonella
bation period, and the hatched chick can then serve sp. can exist simultaneously in a host. Virulent
as a subclinical carrier. In some cases, the salmonella strains are those that can penetrate an intact intes-
infection can eventually induce a septicemia and tinal mucosa, and nonvirulent strains are those that
death. Subclinical carriers allow an infective cycle to require a mucosal lesion to enter a host. Nonvirulent
occur in the absence of other vectors. Vertical infec- strains often colonize the gut, resulting in asympto-
tions may also occur if infected hens feed their young matic infections and intermittent shedding. Once
contaminated crop contents. virulent or nonvirulent strains have passed the mu-
cosal barriers, they induce a septicemia that results
Pathogenesis in an immune response or colonization in tissues and
One of the characteristics of the group Enterobacte- eventual death of the bird. In some cases, Salmonella
riaceae is that they all produce endotoxins. Salmo- sp. may cause chronic infections that are charac-
terized by intermittent septicemia and clinical signs.
Recurrent infections usually result in progressive
TABLE 33.3 Percentage of Psittaciformes Shedding
Gram-negative Bacteria and Yeast
organ involvement; the CNS and joints are fre-
quently end-stage sites of infection.
Pseudomonas
Incubation
Enterobacter
Klebsiella
Incubation periods vary with the type of salmonella

E. coli
Yeast
infection. Presumably, these differences are depend-

Bare-eyed Cockatoo 44 0 0 13 6 ent on the strain of infecting salmonella, the route of
Citron-crested Cockatoo 30 0 0 0 0 infection and the condition of the host. In acute dis-
Major Mitchell’s Cockatoo 27 20 0 0 13 eases, incubation periods are typically three to five
Moluccan Cockatoo 81 13 0 0 13 days. With egg transmission the incubation period is
Sulphur-crested Cockatoo 44 0 0 0 11 shorter, generally considered to be two days. Sub-
Triton Cockatoo 84 8 3 0 0 clinical carriers can have prolonged incubation peri-
Red-vented Cockatoo 78 0 0 0 0 ods.
Umbrella Cockatoo 56 24 4 0 15
Clinical Disease and Pathology
Rose-breasted Cockatoo 16 2 0 0 0
African Grey Parrot 17 0 0 0 0
Acute diseases are characterized by nonspecific signs
Eclectus Parrot 10 0 0 0 10
including lethargy, anorexia, polydipsia (sometimes
Blue-crowned Amazon Parrot 0 0 0 0 0
followed by polyuria) and diarrhea. In subacute to
chronic cases, CNS signs, arthritis (particularly in
Blue-fronted Amazon Parrot 20 0 0 0 0
pigeons), dyspnea and indications of liver, spleen,
Yellow-headed Amazon Parrot 12 0 0 0 0
kidney or heart damage are common. With high-dose
Yellow-naped Amazon Parrot 38 0 0 0 6
infections, conjunctivitis, iridocyclitis and pano-
Blue and Gold Macaw 23 0 0 8 8
phthalmia may occur.
Buffon’s Macaw 23 0 0 8 8
Green-winged Macaw 26 3 0 3 3 Some individual avian species have unique clinical
Military Macaw 20 4 0 0 16 presentations. Outbreaks in lories (Loriidae) and
Red-fronted Macaw 7 7 0 0 0 penguins (particularly Jackass Penguins) are associ-
Scarlet Macaw 19 2 0 0 0 ated with peracute diseases and high flock mortality.
Hyacinth Macaw 6 0 0 0 11 African Grey Parrots are also very susceptible, but
typically develop a more chronic disease exhibiting
Incidence (in percent) of the isolation of gram-negative bacteria and yeast from
the cloaca of a group of psittacine birds with no observed clinical abnormalities. phlegmon, granulomatous dermatitis, arthritis and
Gram-positive bacteria were isolated from 91% of the 506 cloacal samples. It is tenovaginitis (Figure 33.3). Respiratory signs with
not unusual to find transient populations of gram-negative bacteria in the cloaca
of asymptomatic birds. However, the presence of these bacteria in the gastro- myocardial lesions are common in tangares,
intestinal tract can cause problems if a bird is stressed. The isolation of quetzals, Red-headed Barbets, terns and House
gram-negative bacteria from clinically asymptomatic psittacine birds warrants a
close examination of management practices. Adapted from Flammer K: Avian Sparrows. Nonspecific CNS signs are common in
Dis 32: 79-83, 1988.
955
CHAPTER 33 BACTERIA
geese and ducks. Some infected

ducks will swim with an inverted
keel (keel disease) just prior to death.
Subacute salmonellosis in many
finches (Fringillidae) is charac-
terized by granulomatous ingluvitis
that may be confused with candida
infections. Granulomatous dermati-
tis has been reported in several spe-
cies and is thought to be induced by
mosquitoes or other biting insects.
Subgenus III strains are considered

less virulent than those of subgenus
I; however, the clinical lesions in-
duced by this subgenus are indistin-
guishable. Ocular lesions appear to
be more frequent with subgenus III,
and turkeys, ducks, parrots and ca-
naries are particularly susceptible.
Postmortem lesions include dehydra-

tion, degeneration or necrosis of FIG 33.3 A three-month-old pigeon was presented with depression, anorexia, diarrhea
skeletal musculature, gastroenteri- and reluctance to move. An open ulcer was present on the bird’s hock. Salmonella sp. was
isolated from the bird’s feces and the bird responded to treatment with antibiotics
tis (occasionally with ulcers and (courtesy of Louise Bauck).
granulomas), enlargement of the
liver and spleen (with or without dis-
seminated small whitish foci), bile Treatment
congestion and nephropathy. Chronic infections usu-
Whether or not to treat salmonella infections in com-
ally cause pericarditis or epicarditis fibrinosa, granu-
panion birds is controversial. The author believes
loma formation in the liver, spleen and kidney, and
that clinically affected birds and companion birds
degeneration or inflammation of the ovary or testis.
that are identified as carriers should be treated be-
Fibrin filling the cecal lumen is a common finding.
cause of public health hazards. Therapy should in-
Histopathologic changes are nonspecific with puru- clude appropriate antibiotics (based on sensitivity)
lent inflammation in the parenchymal organs. and lactobacillus products. In general, the frequently
Granulomas are common with chronic infections. Pu- encountered salmonella strains are sensitive to com-
rulent leptomeningitis and exudate formation in the monly available antibiotics, but some strains from
subarachnoidal spaces are usually noted in birds free-ranging birds (particularly from seagulls) dem-
with CNS signs. onstrate varying degrees of antimicrobial resistance.
CNS signs and chronic infections tend to be refrac-
Diagnosis tory to therapy. Flock management of salmonella
A confirmed diagnosis requires isolation and identi- should concentrate on preventing egg transmission
fication of the Salmonella species. Serologic evalu- by identifying and removing subclinically infected
ation of a flock can be used only if the precise species breeders. Treating birds that have egg-derived infec-
is known; however, chronically infected subclinical tions is extremely difficult. Host-adapted strains of
birds are frequently serologically negative. The same salmonella seem to cycle in periods of approximately
is true for birds infected with L-forms. The develop- three-month intervals. Cycles of egg transmission
ment of a serologic response requires penetration of can best be broken by collecting eggs for future breed-
the intestinal mucosa, and most subclinical carriers ing stock four weeks after treating the parent stock.
have infections limited to the intestinal lumen. Newly hatched chicks from these birds should be
cultured (fecal swabs) at hatching, and infected birds
should be treated immediately.
956
freundii antibodies often cross-react with those to S.

typhimurium.
Citrobacter spp. cause serious secondary infections in

weaver finches and waxbills. A rapid bacteremia fol-
lowed by acute death occurs when the organism
penetrates the intestinal mucosa. Ostriches, particu-
larly chicks and young birds, also appear to be very
susceptible to Citrobacter spp. Infected birds of any
species may die without any clinical signs, or they
can exhibit a brief period of depression and diarrhea
prior to death. Postmortem changes indicate septice-
mia (petechiation of the heart, musculature and pa-
FIG 33.4 Aviary hygiene is important in preventing a bird’s expo- renchyma). Surviving birds frequently become carri-
sure to many infectious agents including bacteria. Walk-in type ers. C. amalonaticus is frequently recovered from the
enclosures have several disadvantages when compared to drop-
through type enclosures. The birds in walk-in enclosures can fly to
intestinal tract of normal Psittaciformes. Intestinal
the floor where pathogens can accumulate in excrement and food infections would indicate that a disturbance has oc-
waste. Birds are more likely to come in contact with discharge from curred in the autochthonous flora. A definitive diag-
flies or rodents that have ready access to organic waste on the floor
of the enclosure. Additionally, caretakers can act as mechanical
nosis requires culturing the organism from affected
vectors for the transmission of pathogens as they walk from one tissues. The rule-out list is the same as for Salmo-
enclosure into the next. nella spp. Therapeutic decisions should be based on
appropriate culture and sensitivity. Neomycin deliv-
ered by gavage is often effective in clearing intestinal
Treatment of L-forms can be attempted with clin-
infections. In flock outbreaks, the same drug admin-
damycin (100 mg/kg body weight) or a combination of
istered in the drinking water may be helpful in con-
erythromycin and ampicillin (both components at the
trolling infections.
full dose).
There have been no reported cases of citrobacter
Control
infections in humans derived from exposure to in-
Proper hygiene is the best tool for preventing salmo- fected birds.
nella outbreaks. The effective control of flies, rodents
and other vermin is essential (Figure 33.4). Regular
cleaning and disinfection of the aviary and nursery, Klebsiella (K.)
along with proper storage of food, are all important K. pneumoniae and K. oxytoca are frequently recov-
in preventing salmonellosis. Several Salmonella spp. ered from birds in which they can function as pri-
vaccines have been evaluated experimentally, but mary pathogens, particularly in weaver finches, or
none have proven to be effective. they can be involved as opportunists in immunosup-
Companion bird strains of Salmonella are not consid- pressed or stressed patients. These organisms are
ered important human pathogens in healthy indi- nonmotile Enterobacteriaceae, and most members of
viduals, but can cause problems in infants, geriatric the genus are encapsulated. The mucoid capsule pro-
patients or those with immunosuppressive diseases. vides them with substantial protection from environ-
Humans carrying salmonellosis can infect their com- mental extremes and many disinfectants. Heat and
panion birds. Such human-to-animal interactions drying are the best methods of killing Klebsiella spp.
have been shown to occur with African Grey Parrots, Specific information on the transmission, pathogene-
Amazon parrots, cockatoos and macaws. sis and incubation period for Klebsiella spp. in birds
is not available. The Klebsiella capsule provides a
Citrobacter (C.) barrier to protect the organism from cellular immu-
nity. However, the capsule is also highly antigenic
The three species of Citrobacter (C. freundii, C. and stimulates a protective humoral immune re-
amalonaticus and C. diversus) are less commonly sponse. Klebsiella spp. bacteremia usually results in
encountered than other members of the Enterobacte- the colonization of the kidney, causing renal failure.
riaceae. C. freundii appears to be the most patho- In chronic infections, the lungs may also be involved.
genic of the group. C. diversus is rare in birds. When In many bird groups (eg, pigeons, weaver finches,
using serologic assays it is important to know that C.
957
CHAPTER 33 BACTERIA
goldfinches and siskins, geese, birds of prey, Amazons Clinical Disease and Pathology
and African Grey Parrots), infections are not de- Y. pseudotuberculosis may be associated with per-
tected until late in the disease process when respira- acute, acute or chronic clinical disease. Peracute
tory signs occur. Encephalomyelitis is occasionally death without clinical signs is common in infected
noted in terminal cases. While systemic klebsiella Piciformes and Musophagidae. Clinical signs associ-
infections are most common, local infections involv- ated with acute disease include lethargy, dehydra-
ing the sinuses, skin, oral cavity and crop may also tion, diarrhea and dyspnea. Emaciation, wasting and
occur, particularly in Psittaciformes. The diagnosis is flaccid paresis or paralysis are common with sub-
made by isolation and identification of the organism. acute or chronic cases. Birds with a wasting syn-
The rule-out list is the same as with salmonella. drome appear similar to animals infected with tuber-
culosis. Infected ducks frequently develop tarsal joint
Yersinia (Y.) swelling. Canaries may be severely dyspneic prior to
death.
The genus Yersinia currently consists of eleven spe-
cies.1 Unlike other Enterobacteriaceae, which are Gross changes associated with peracute infections
strictly rod-shaped, Yersinia spp. form ovoid-to-coc- include swelling of the liver and spleen and bloody-
coid rods that replicate in the environment at ex- to-fibrinous exudate into the body cavity. Submiliary-
tremely low temperatures (+4°C) if provided the to-miliary, sharply demarcated grayish foci within
proper sources of organic nitrogen. Because the or- the liver, lungs, spleen and kidneys are common with
ganism can grow effectively at low temperatures, the acute course. Chronic infections are charac-
infections are particularly common during the winter terized by granuloma formation in organs and the
months. skeletal musculature. Ascites and osteomyelitis may
or may not be present. Ulcers in the proventriculus,
Y. pseudotuberculosis appears to be the most impor- ventriculus and duodenum may occur in infected
tant avian pathogen. Y. intermedia, Y. frederiksenii canaries. Tarsitis chronica deformans with caseous
and Y. kristensenii are frequently isolated from vari- exudate in the joint cavity is frequently seen in
ous avian species, but their pathogenicity remains ducks.
undetermined.
Coagulation necrosis and thrombophlebitis are the
When grown at 20-28°C, Y. pseudotuberculosis is mo- common histologic changes. In acute and chronic
tile; when grown at higher temperatures it is nonmo- cases, inflammatory cells infiltrate the necrotic areas
tile. Six serovars have been distinguished. Serovar 1 and eventually induce granulomas.
is most frequently isolated from birds. Y. pseudotu-
berculosis has been recovered in an L-form from free- Diagnosis
ranging urban pigeons. The histopathologic changes, along with the identifi-
cation of gram-negative coccoid rods, are suggestive
Transmission of Y. spp. infections. Definitive diagnosis requires
Y. pseudotuberculosis is thought to be indigenous to isolating the organism from affected tissues. Placing
northern and middle Europe. The occurrence of this contaminated samples in a cool environment for two
bacterium in other parts of the world including Can- weeks may help in recovering Y. spp. Isolating avian
ada, the United States, Africa and Australia is strains of yersinia appears to be more difficult than
thought to have arisen from the movement of Euro- isolating mammalian strains. Because there are no
pean birds and rodents to other suitable geographic demonstrable biochemical or serologic differences, it
locations. An unknown percentage of the free-rang- has been assumed that avian strains are more diffi-
ing birds in Europe are considered asymptomatic cult to grow due to different nutritional require-
carriers. ments. The most consistent isolation results have
been obtained by placing fecal or organic material in
Y. pseudotuberculosis infects a wide range of hosts, heart-infusion broth with 5% glucose and storing this
including many bird species and various mammals, material in a refrigerator for two weeks. The mate-
particularly rodents and including humans. Toucans, rial is then inoculated on blood agar plates with 0.2%
toucanets, aracaris, barbets and turacos appear to be Tween 80 and 50 ppm tellurite and incubated at 37°C
extremely susceptible. for two days. Yersinia causes a reduction of the tellu-
rite, turning the colonies black.25
958
Treatment Both of these bacteria infect many mammals, includ-

Birds with the peracute to acute forms of yersiniosis ing humans, as well as most of the birds that have
usually die before therapy can be instigated. Paren- been tested. Free-ranging waterfowl appear to be
teral drug administration is required if therapy has particularly susceptible, but any free-ranging avian
any chance of being successful. Treating chronic species that contacts contaminated food or water is
cases is difficult because granulomas prevent antibi- probably susceptible. Of the commonly maintained
otics from reaching the yersinia organisms nestled in zoo birds, penguins are very susceptible.
the center of necrotic debris. Flock outbreaks can be
prevented by treating clinically unaffected animals Pathogenesis
and applying strict sanitary measures. Some strains of Pseudomonas and Aeromonas pro-
duce a number of extracellular toxins, including
Control hemolysins, elastase, protease and lecithinase, that
In non-European countries where Y. pseudotubercu- cause cellular damage resulting in edema, hemor-
losis is not endemic, repeated culture of feces during rhage and tissue necrosis. Avian strains of Ae. hydro-
the quarantine period should be used to prevent phila that are acetoin-producing (Voges-Proskauer-
infected birds from entering the country. In endemic positive) are considered to be highly toxic.6 Both
areas, rodents and free-ranging birds can serve as species are principally secondary invaders. However,
reservoirs, and flock control depends on preventing the toxins secreted by these organisms can be life-
these animals from contaminating feed supplies and threatening once colonization of the host occurs. Ps.
keeping them out of the aviary. Several experimental aeruginosa is resistant to many commonly used anti-
vaccines for Y. pseudotuberculosis have proven to be biotics and can cause secondary superinfections in
ineffective. Feeding infected mice to toucans could patients being treated for other bacterial infections.
serve as a source of infection.
Y. enterocolitica is principally a human pathogen. Virulent strains of these bacteria can cause a septi-
Gulls, herons, birds of prey, crows, blackbirds and cemia that induces diarrhea, dehydration and dysp-
European robins that inhabit areas contaminated nea followed by acute death. Infected skin lesions are
with human sewage are frequently infected. Young edematous or necrotizing. Localized infections may
children of elementary school age are particularly occur in the upper respiratory tract, causing rhinitis,
susceptible to infections. sinusitis and laryngitis. Hemorrhages and coales-
cent necrosis in the liver, spleen and kidney are the
Pseudomonas (Ps.) and Aeromonas (Ae.) most common postmortem findings (see Figure 33.2).
Catarrhal to hemorrhagic enteritis with edema and
These two gram-negative rods are taxonomically un- fibrinous inflammation of the serosal membranes
related but nevertheless have characteristics that may also be noted. Histologic changes associated
make it best from a clinical perspective to discuss with infections include severe inflammatory reac-
them together. Both of these genera contain numer- tions involving the venous and arterial walls. Bacte-
ous species, but only Ps. aeruginosa and Ae. hydro- ria are often identifiable within the lumina. The
phila are common avian pathogens. Both bacteria formation of thrombi, hemorrhage and necrosis of the
are frequently found in aquatic environments and infected vessels are the results.
can propagate in cool water (20°C or lower). Both
bacteria will grow on common media and induce Diagnosis and Control
β-hemolysis on blood plates. These hemolysins are The causative agent should be isolated and identi-
potent toxins and are capable of damaging many cells fied. Aviary outbreaks of pseudomonas are most com-
in addition to erythrocytes. Ps. aeruginosa produces mon when organic material contaminates the water
a blue-green diffusible pigment and has a sweetish supply, allowing a proliferation of the organisms in
odor. Ae. hydrophila causes the typical bad smell of the drinking water (Table 33.3). Routine cleaning of
the proteinolytic organisms and may be confused food and water containers, along with any external
with E. coli on Endo- or MacConkey plates. These water pipes, is an important control measure. Incu-
bacterial genera are further divided into several se- bator contamination can be prevented by periodically
rovars and biovars. There have been insufficient cleaning the water reservoir. Waterfowl are particu-
studies to divide the avian species in a similar fash- larly susceptible to infections when water tempera-
ion. tures are above 20°C, allowing rapid proliferation of
959
CHAPTER 33 BACTERIA
Ae. hydrophila. Removing waterfowl from ponds dur- noncholera Vibrio can be recovered from healthy
ing these periods is a good control measure. birds.
C. jejuni may appear in different forms including a

Alcaligenes (Ac.) and Bordetella (Bo.) short comma, s-shaped, long spiral or coccoid form.
The genera Alcaligenes and Bordetella are taxonomi- The latter is usually an indication of degeneration.
cally related. Both genera are widely spread in the Colony formation takes 72 to 96 hours at 37-42°C in
environment. Alcaligenes is found mainly in aquatic a microaerobic environment. Blood agar or selective
environments. Ac. faecalis, Bo. avium and Bo. bron- media are best for isolation. C. jejuni is relatively
chiseptica infect a wide variety of birds in many unstable in the environment (surviving less than one
orders. Psittaciformes and turkeys as well as many week).
finches seem to be particularly susceptible to these
There are at least 50 serovars of C. jejuni.42 While the
bacteria.
possibility of birds serving as a source of infection for
There are no details on the pathogenicity of these mammals and vice versa has been discussed, this
genera in birds. Alcaligenes and bordetella are oppor- transmission potential has been insufficiently stud-
tunistic pathogens that potentiate viral and other ied.
bacterial infections. Bordetella avium, a more re-
The host spectrum is large, and includes chickens,
cently recognized member of the genus, seems to
turkeys, pheasants, crows, gulls, ducks, geese, pi-
preferentially bind to the ciliated epithelial cells of
geons, shorebirds, Pekin Nightingale, Nandu and the
the upper respiratory tract.
Great Bustard. C. jejuni has recently been reported
In turkeys, combined infections of Bo. avium and the in passerine birds, particularly in tropical finches
turkey rhinotracheitis virus cause the clinical and (Estrildidae) and, to a lesser degree, in canaries.20
pathologic signs of rhinotracheitis. In other avian Details of occurrence and pathogenicity in many
species, clinical signs are uncommon and, if present avian species have been reported.51 Psittaciformes
at all, are nonspecific. At necropsy, tracheitis, bron- are susceptible, but few documented infections have
chopneumonia and air sacculitis are common find- been reported.
ings with subacute to chronic courses of bordetella,
Pathogenesis
whereas alcaligenes infections are characterized by
coalescent liver necrosis in addition to respiratory C. jejuni can be isolated from the intestinal tract of
disease. clinically affected and asymptomatic birds. Experi-
mental infections generally cause hepatitis. Factors
Diagnosis that determine if an infected bird becomes clinically
A confirmatory diagnosis requires isolation and iden- affected have not been established. Clinical disease
tification of the causative agent. Serologic flock diag- is common in birds with parasitic infections (coccidia
nosis by means of the slide agglutination test or and nematodes), and these agents have been sug-
antibody titration by the Gruber-Widal method is gested as predisposing factors.
possible although no commercial antigens are avail-
able.
Clinical signs are generally associated with subacute
to chronic hepatitis and include lethargy, anorexia,
Campylobacter (C.) diarrhea (frequently with yellowish stained feces)
and emaciation. Transmission takes several weeks
Campylobacter spp. from birds have been classified
through the flock, but spontaneous recovery and re-
as: C. jejuni, the most frequent, and probably also the
lapses do occur. High mortality has been noted in
most pathogenic; C. coli, which is considered to be
finches, especially among fledglings.20 Sudden death
apathogenic, but is frequently confused with C. je-
as a result of liver rupture is possible. Heterophilia
juni; and C. laridis, which is isolated from gulls,
and thrombocytophilia are the most consistent
whose pathogenicity is still not definitely known.36
changes in the CBC.
C. jejuni has incorrectly been labeled as Vibrio (usu-
At necropsy the liver is enlarged, pale or greenish in
ally V. metschnikovii). This error has serious conse-
color and is congested, with or without hemorrhage.
quences because Vibrio cholerae, serotype 01 and
Perivascular infiltrates make the lobules appear
more prominent. Coalescing necrotic hepatitis is a
960
common histologic finding. Catarrhal enteritis (also Transmission

hemorrhagic enteritis in pheasants, turkeys, Teng- The main vectors for transmission are ticks, in which
malm’s Owl and coot) has been described. In gulls, the organism can be passed transovarially and sur-
erosion of the ventriculus has been reported. vive for over a year. Mosquitoes and other biting
insects play a minor role in transmission. Transmis-
Diagnosis sion from bird to bird by excreta is of minor impor-
Diagnosis requires isolation of C. jejuni from affected tance epizootiologically.
tissues. Phase-contrast microscopy of bile to demon-
strate suggestive organisms may provide a tentative Pathogenesis
diagnosis. Fecal samples can be used for culture in Young chicks (one to three weeks of age) are particu-
live birds. A transport medium is necessary to ensure larly susceptible. Adults may also be infected. Bor. is
survival of the organism. in the peripheral blood from the fourth to the ninth
day post-infection and remains in the blood approxi-
Treatment and Control mately seven days. The organism can then be found
There are discrepancies between the antibiograms in parenchymal organs for another 30 days. Death
and clinical recovery. Erythromycin or tetracyclines, may occur from embolism due to agglutinating borre-
dehydro- or streptomycin (never in Psittaciformes) or lias. A strain-specific immunity develops in survi-
furane derivatives (not in waterfowl) can be tried. vors. Incubation periods are four to eight days de-
Diseases frequently recur despite therapy. Thorough pending on the species of ticks.
cleaning and disinfecting of the aviary may help
prevent reinfection. Dogs can be a reservoir for hu- Clinical Disease and Pathology
man infections, but it is not known if they can trans- Acute cases are characterized by a high fever (bacte-
mit the organisms to birds. Dogs should not be al- ria generally cause a low body temperature), ano-
lowed direct access to birds. rexia, depression (droopy, cyanotic heads), yellowish
diarrhea, lethargy, ataxia and paralysis. Morbidity is
Vibrio (V.) high, and mortality may range from 10 to 100%
depending upon the susceptibility of the host. Spon-
The genus Vibrio comprises numerous species that taneous recovery may occur around the sixth day
are not easy to differentiate. V. cholerae is of utmost post-infection. Chronic disease is characterized by
importance as a zoonotic organism. In birds, espe- anemia, paralysis and dyspnea.
cially in gulls, V. cholerae (serovar 01) is demonstra-
ble in the intestinal tract, although no clinical or The albumin fraction in the serum decreases to 37%
pathologic signs have been described. Numerous and an increase of the aspartate aminotransferase is
other V. spp. are collectively designated NAG (= non- accompanied by a decrease of the alkaline phos-
agglutinable), because they do not agglutinate with phatase, the total lipids and the cholesterol.
human cholera antiserum. NAG strains can be iso-
lated from the feces of many bird species, particu- At necropsy, a mottled, severely enlarged liver is
larly waterfowl (vibrio is generally found in aquatic characteristic except in pheasants. In these birds the
habitats).4 NAG vibrios have not been documented as spleen may be small or normal in size.58 The liver
a cause of clinical disease in any avian species. Be- shows hemorrhages and necrotic foci. Mucoid hemor-
cause some NAG strains can cause a mild intestinal rhagic enteritis, serofibrinous pericarditis and swol-
disease in humans, an analysis of avian strains in the len kidneys may also be seen. Histology displays
vicinity of human cases might be advisable. multiple necrotic foci without inflammatory reac-
tions. Bor. can be demonstrated by argentation.
Spirochaetaceae Diagnosis
Blood smears stained with Giemsa or examined by
Borrelia (Bor.) anserina (syn. Spirochaeta gallina-
darkfield microscopy are useful for diagnosis. Cultur-
rum) is a gram-negative, helical motile organism that
ing Bor. sp. is very difficult. Antibodies (agglutina-
stains with Giemsa. A granular form of the organism
tion, fluorescence techniques, immunodiffusion) can
may occur in ticks and the blood of the birds that
be demonstrated from the 4th to the 30th day post-
have recovered from a disease. The host spectrum
infection.
includes geese and ducks, turkeys, chickens, pheas-
ants, grouse, partridges, pigeons, crows, magpies,
House Sparrows, starlings and African Grey Parrots.
961
CHAPTER 33 BACTERIA
Treponema (T.) spp.: Treponema spp. are helical taxonomically classified. Some isolates designated P.
motile organisms that are much smaller than Spiro- haemolytica (gram-negative, polymorphic rods) are
chaeta spp. An unclassified Treponema sp. (0.5 µm improperly classified and do not belong in this genus.
wide with 13 to 15 flagella)12 is the cause of a watery, The characteristics of these strains resemble those of
intermittent typhlitis in chickens. The organism is the genus Actinobacillus. Reports on isolation of P.
antigenically related to but distinct from T. hyodysen- pneumotropica from birds are questionable. This spe-
teriae. Chickens are the only defined host and lose cies appears to be host-specific and is found in rats or
weight in response to a malabsorption syndrome.12,22 other rodents. Similarly, P. ureae is believed to be
Histopathology shows an increased number of goblet host-specific for humans.
cells in the cecal mucosa, focal epithelial desquama-
tion and many Treponema organisms in the small Pasteurella has been associated with disease in Pha-
fissures of the epithelium. The incubation period is sianiformes, Anatiformes, Psittaciformes, Columbi-
one to seven weeks dependent on the infective dose. formes and Passeriformes. There is variance in spe-
Culture is possible on spectinomycin blood agar in an cies susceptibility. The clinical presentations and
anaerobic atmosphere. Fluorescent antibodies de- pathomorphologic changes are similar to those de-
signed for T. hyodysenteriae can be used to demon- scribed for yersiniosis. Propagation outside the host
strate the organisms in affected tissue. can occur but requires very specific conditions of
temperature, relative humidity and pH. Such condi-
Spirochaetaceae Undifferentiated: A non-classified tions may occur in large bodies of water, and in these
spirochete from choanal and tracheal mucus of a situations Pasteurella spp. can survive for long peri-
cockatiel has been described. The organisms were 0.3 ods. Epornitics are most common in the northern
to 0.4 X 10 to 15 µm in size and occurred in large hemisphere from November to December. Outbreaks
numbers on the mucosa. Two other cockatiels have in tropical climates peak with seasonal highs in am-
been found to harbor similar organisms in the respi- bient temperature and humidity.
ratory passage. Histopathology showed a mild in-
flammatory reaction in the nasal sinus, but not in the P. multocida: The etiologic agent of fowl cholera, the
trachea. In the lower parts of the respiratory tract, species is divided into strains based on 16 serologi-
the organisms could not be demonstrated using ar- cally distinct endotoxins and 4 capsular polysaccha-
gentation. The significance of these findings is un- rides. Serotypes 1 and 3 and capsule types A and D
known. Interference with the ciliary activity of the are most commonly isolated from birds. Three sub-
respiratory mucosa is conceivable.65 species, P. multocida (m.) multocida, P. m. galli-
narum and P. m. septica, have been distinguished
Spirochetes were demonstrated in a pharyngeal based on differences in virulence. The latter is con-
swab of a cockatiel that was depressed and sneezing. sidered to be the most virulent.
The bird had spent ten minutes with another cocka-
tiel that was showing similar clinical signs ten days P. pneumotropica is indigenous in rodents and occa-
before being presented for evaluation. sionally causes disease in aviary birds and pigeons.
Infected birds develop pneumonia and may exhibit
dyspnea shortly before death. Detailed information
Pasteurella (P.) on the pathogenesis and clinical progression of P.
pneumotropica in companion birds has not been re-
The family of Pasteurellaceae currently includes the
ported.
genera Pasteurella, Actinobacillus and Haemophi-
lus.49 All three genera can be pathogens in birds. P. gallinarum appears to have a similar host spec-
trum as P. multocida; however, P. gallinarum is
Pasteurella characteristically exhibit bipolar stain-
thought to be much less pathogenic. If the organism
ing in tissue smears or from first culture passages
is able to colonize the respiratory mucosa, it can
when fixed in methanol and stained with methylene
induce conjunctivitis and respiratory signs including
blue. There are presently eleven species within this
coryza, rales and dyspnea. P. gallinarum has been
genus, but others will undoubtedly be added. P. mul-
isolated from the choanae and nostrils of Psittacifor-
tocida, which causes fowl cholera, and P. gallinarum
mes with concomitant Aspergillus spp. infections in
are two of the most commonly encountered species.
the lungs and air sacs. Aspergillosis is one of the
The latter is usually considered a secondary patho-
triggering factors that allows this secondary patho-
gen. Some of the Pasteurella organisms isolated from
gen to overcome host defenses. Postmortem findings
waterfowl, pigeons and Psittaciformes have not been
associated with P. gallinarum include catarrhal to
962
produced by Pasteurella damage blood vessels, caus-

ing edema, hemorrhage and coagulation necrosis,
particularly in the liver. Diseases by less virulent
strains usually occur in stressed or immunocom-
promised hosts.

Acute forms are characterized by cyanosis, dyspnea
and diarrhea followed by death. Excess mucus may
be present around the nostrils or beak. Birds that
survive 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 the
parenchymal organs. Prolonged cases are charac-
FIG 33.5 The hallmark sign of bacterial septicemia is depression. terized by exudative serositis (mainly white, in con-
Birds that are bitten or scratched by cats frequently develop P. trast to yellow with E. coli) and the formation of
multocida bacteremia. Affected birds may appear normal immedi- necrotic foci in infected organs. Catarrhal to fibri-
ately after the injury occurs, and become rapidly depressed and die
12 to 24 hours later. Any carnivore-related injury in a bird is a nous rhinitis, necrotic pneumonia, sinusitis, ble-
critical emergency. pharoconjunctivitis and tracheitis are common with
chronic courses. Following bacteremia, Pasteurella
may colonize numerous tissues, resulting in arthri-
fibrinous inflammation of the upper respiratory tis, osteomyelitis, otitis media and granulomatous
tract, pneumonia and air sacculitis. dermatitis. Granulomas may also be noted in the
Transmission liver and spleen. Some strains will colonize the air
cells of the cranial bones causing fibrinous exudate.
Pasteurella infections in birds principally occur in
In waterfowl, a diphtheroid enteritis may be ob-
the respiratory tract. Asymptomatic carriers harbor
served. Histologic changes are nonspecific.
the bacteria in the nasal cavities, sinuses and cho-
anae. Transmission can occur through direct contact Diagnosis
with contaminated aerosols or through mechanical The isolation of the causative agent is necessary. The
vectors such as blood-sucking mites. Infected rodents occurrence of Pasteurella spp. in a flock can be deter-
and free-ranging birds are considered important res- mined through serology using immunodiffusion or
ervoirs. Pasteurella is shed almost exclusively from indirect hemagglutination tests. Unfortunately, com-
the upper respiratory tract. Shedding in the feces is mercial antigens for these tests are not available.
rare, and egg transmission has not been documented. Serotyping and differentiation of the subspecies re-
P. multocida is a common inhabitant of the oral quire specialized testing.
cavity of some carnivores, particularly cats, and sep-
ticemic infections can occur through bite wounds. Treatment
Cats should always be considered to be carriers of P. Septicemic birds rarely survive, even when treated
multocida, and any bird that has been mouthed by a intensively. Parenteral administration of broad-spec-
cat should be treated with antibiotics immediately trum, long-acting sulfonamides can be tried. The
(Figure 33.5).40 combined use of antibiotics and hyperimmune serum
has proven to be beneficial. Treating birds with
Pathogenesis
chronic forms is very difficult because of the irre-
Virulent strains of P. multocida cause an acute septi- versible damage that occurs to parenchymal organs.
cemia and death. Less virulent strains result in bac-
teriemia and colonization of the lungs, liver, kidneys, Control
spleen and heart. Weakly virulent strains generally Preventing rodents and free-ranging birds from en-
cause a chronic respiratory disease. The endotoxins tering the aviary is important in preventing infec-
963
CHAPTER 33 BACTERIA
tions. Vaccines for P. multocida are commercially signs developing in goslings each season. At necropsy,
available, but their effectiveness is poor. Failures liver necrosis, salpingitis, peritonitis, endocarditis
associated with the vaccine occur because of the nu- valvularis and fibrinous arthritis are typical lesions.
merous different serotypes and the fact that endotox- In young geese, polyserositis and arthritis are promi-
ins are more immunogenic than the bacterial cap- nent.
sule. The production of vaccines from strains that
persist in an aviary may provide successful long- Diagnosis and Treatment
term control. Isolation and identification of the causative agent is
necessary for diagnosis.
Actinobacillus (At.) E. coli and other bacteria, particularly anatipestifer
The genus Actinobacillus consists of a group of organ- infections in waterfowl, have to be considered as
isms provisionally differentiated into more than 20 causative agents for the salpingitis, peritonitis and
biovars, some of which have a rather high host speci- polyserositis.
ficity. The taxonomic reclassification of the Pas- Tetracyclines and chloramphenicol are indicated for
teurellaceae is intertwined with the genus Actino- initial therapy. Sensitivities for many strains are
bacillus. Because of these classification revisions, difficult to interpret because of oversized inhibition
even the actinobacilli that are pathogenic in birds zones. In young geese, antibiotics must be given
have not been named. The situation has been compli- during the first week of life or lesions become too
cated in recent years because many new strains have extensive to be reversed.
been isolated from Psittaciformes, Columbiformes,
Anatiformes and Fringillidae. One biovar has been
referenced in the literature as P. haemolytica syn. At. Haemophilus (H.)
salpingitidis. However, this classification is not
The haemophilus strains that infect companion birds
valid. The knowledge of the biology and pathogenic-
have not been properly classified. Chickens are con-
ity of the members of the genus is limited.
sidered to be the only definitive host of H. paragalli-
Actinobacilli are polymorphic rods that may exhibit narum, which is the agent of coryza contagiosa galli-
bipolar staining similar to Pasteurellae. Most strains narum. Experimentally, Columbiformes and
grow only on blood agar plates or media containing Anatiformes are resistant to infection. Several
serum. Some strains, particularly of At. salpingi- Haemophilus spp., including H. avium a n d H.
tidis, hemolyze avian and bovine erythrocytes or pro- paravium, can be isolated from birds with coryza;
duce exotoxins that are capable of causing arteritis. however, their involvement in the disease process is
Some strains are considered to be primary patho- questionable. They probably serve as secondary in-
gens, but the majority of this genus is comprised of vaders that sustain upper and sometimes lower res-
opportunistic organisms. There are no simple labora- piratory tract disease.11,35
tory tests for differentiation between primary and
Pathogenesis
secondary invaders.
Details on the pathogenesis of Haemophilus spp.
There is little information on routes of transmission. strains that infect Psittaciformes and Columbifor-
It has been proven that egg transmission of some mes are scarce. H. paragallinarum is known to pro-
strains occurs in chickens and geese. Incubation pe- duce a number of cellular toxins, including neu-
riods in the avian host are not known. raminidase, nitratase and catalase. Birds do not
appear to develop an immune response following
Clinical Disease and Pathology infection, and relapses are common.
Many infected birds die acutely. Birds with a more
chronic course typically develop joint lesions. Spe- Clinical Disease and Pathology
cies-specific strains that infect geese morphologically Haemophilus infections generally cause a rhinitis
resemble P. influenzae. This organism has been ref- that results in a serous-to-mucoid or even fibrinous
erenced as a cause of chronic disease in the gosling,26 exudate. Conjunctivitis and sinusitis may also occur.
characterized by emaciation, failure to thrive, poor The most common postmortem finding is catarrhal-
feed conversion and arthritis. Egg transmission may to-fibrinous rhinitis. Bronchopneumonia and air sac-
cause reduced hatchability. Asymptomatic infections culitis are frequently described but are usually the
are thought to occur in adult breeders, with clinical result of concomitant infections (virus, other bacte-
964
ria, Candida spp.). For those lesions supposedly and the condition of the host must also play a role.
caused by Haemophilus spp. apart from H. paragalli- The incubation period in ducks ranges from three to
narum see Table 33.4.32,35 Histopathology reveals un- ten days.
characteristic lesions.
TABLE 33.4 Clinical Disease Caused by Haemophilus in Avian Species
Infected ducklings (two weeks of age) usually die
peracutely. Mortality rates in this age group can
Blue Crane Pneumonia (together with staphylococci) reach 75% of exposed young. Acute disease develops
and necrosis of liver tissue
in older birds and is characterized by sinusitis, con-
Pigeon Rhinitis
junctivitis, coughing and diarrhea, followed in two
African Grey Parrot Pneumonia, air sacculitis days by tremors, ataxia and convulsions. Survivors
Plum-headed Parakeet Sinusitis, swelling of the liver together are stunted and fail to grow. Fibrinopurulent polyse-
with E. coli or related organisms
rositis is the characteristic postmortem finding.
Eastern Rosella Sinusitis, swelling of the liver together
with E. coli or related organisms Other changes include lung congestion, hepa-
Budgerigar Rhinitis (possibly together with tomegaly, splenomegaly, pericarditis and perihepati-
Pasteurella or E. coli) tis. Cytophaga-induced spondylitis with compression
Muscovy Duck Rhinitis, sinusitis of the spinal cord was reported in turkeys.10 Diffuse
Andean Goose Rhinitis, hemorrhage, jejunitis fibrinous meningitis with lymphocytic infiltration
Turkey Sinusitis, air sacculitis around the meningeal blood vessels was a charac-
Golden Pheasant Sinusitis, diphtheroid surface lining of teristic histologic lesion. There was exudate forma-
the beak cavity tion within the ventricles as well as proliferation of
Siamese Fireback Necrosis of the lung tissue. microglia in the subpial and periventricular
system.
Diagnosis
The occurrence of polyserositis is highly suggestive of
an infection. Isolation and identification of the causa-
Other Gram-negative Rods tive agent is necessary in all other cases. An ELISA
can be used to survey a flock for serologic response.
Tularemia
New Duck Disease (Duck Septicemia)
Tularemia is caused by Francisella tularensis, a mo-
The etiologic agent of duck septicemia has been sus- tile, short rod, 0.2 X 0.3-0.7 µm in size. Isolates are
pected to be Pfeifferella, Pasteurella or Moraxella reported occasionally, mainly from birds that inhabit
anatipestifer. The causative organism has recently the northern and subarctic regions of the northern
been placed in the genus Cytophaga, which is a hemisphere, such as the Common Pheasant, Wax-
semiaerobic, nonmotile rod.49 The genus contains at wing, Ural Owl, Rough-legged Hawk and Common
least 19 serovars; serovars 1-3 are most common in Raven. Rodents are considered to be the primary
Europe; serovars 1, 2 and 5 are most common in the reservoir. Nothing is known about the clinical signs.
United States; serovar 3 is frequently isolated in The pathology resembles that of Pasteurella or
Australia. This organism is known to infect ducks Yersinia infections. Francisella previously has been
and geese, free-ranging waterfowl, turkeys, pheas- classified with these two genera. The organism is
ants and Psittaciformes. There is no information on considered to be a zoonotic agent.
its virulence or ability to survive in the environment.
Experimental disease does not occur following oral Acinetobacter calcoaceticus (An.)
administration, and the respiratory tract is thought
This organism forms either cocci (fresh culture) or
to be the primary portal of entrance to the host. Egg
rods. It grows on commonly used media, even on
transmission resulting in high morbidity and mortal-
some selective media for Enterobacteriaceae. The
ity of ducklings is a substantial factor for the flock.
host spectrum is wide, and many avian orders can
The pathogenicity of cytophaga is undetermined. Un- harbor the organism in the respiratory or intestinal
doubtedly, there are strain differences in virulence, tracts. Egg transmission is possible in many avian
species. No reports conclusively describe consistently
965
CHAPTER 33 BACTERIA
occurring lesions in any avian species. Therefore, it studied sufficiently to determine their importance in
is assumed that the organism has a low pathogenic- birds. Staphylococcus protein A, which is found in the
ity, and infections indicate a compromised host. bacterial cell wall, is capable of binding to the Fc-
fragment of immunoglobulin, thereby inhibiting
phagocytosis of the organism. The correlation be-
tween protein A production and the virulence of
avian Staphylococcus strains is poorly documented.
Gram-positive Bacteria Members of the genus Staphylococcus (apart from S.
of Clinical Significance aureus) are commonly recovered from many avian
species and are considered part of the autochthonous
flora. When present in diseased tissue, they are gen-
erally considered to be secondary invaders. Because
Staphylococcus (S.) S. aureus includes the most virulent strains, the
following discussion applies mainly to this species.
Staphylococcus infections can induce sporadic or en-
zootic disease in many avian species. Clinical mani-
festations may include acute septicemia or subacute- S. aureus
to-chronic arthritis, osteomyelitis and osteitis. Less
Avian strains of virulent S. aureus are relatively
common clinical problems include vesicular dermati-
species-specific and rarely induce disease in mam-
tis or omphalitis. Staphylococci, particularly S.
mals. The organism is found in abundant quantities
aureus, can function as primary pathogens or may
in air and dust. Isolation of the organism can fre-
complicate other infections as secondary invaders.
quently be accomplished from the skin and the mu-
Isolation of the staphylococci is relatively simple us- cosa of the respiratory or digestive tract of clinically
ing common media and growth conditions. Taxonomy normal birds (Figure 33.6). S. aureus, like other
literature50 currently lists 21 Staphylococcus spp., 14 Staphylococcus species, is relatively stable in the
of which can be found in birds and are given here in environment and can remain infectious for long peri-
order of decreasing frequency. S. xylosis is considered
almost apathogenic. S. sciuri and S. lentus (the latter
a former biovar of S. sciuri) have some pathogenicity
markers. S. aureus includes more virulent strains
than any other species. These four Staphylococcus
species are further divided into several biovars. Be-
cause some of these biovars are recovered only in a
limited number of closely related bird species, they
may represent bacterial organisms that have
adapted 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 earlier
literature but, using current diagnostic tools, is today
rarely found in birds. The isolation of these less
common species frequently depends on the internal
or external environment of the patient, and limited FIG 33.6 A five-year-old Amazon parrot was presented with an
information is available concerning their pathogenic- acute onset of picking at the feet and legs, which caused hyperemia
ity. and scab formation. This syndrome, called Amazon foot necrosis,
has been reported in Amazona spp., and Staphylococcus spp. are
frequently isolated from the lesions. However, staphylococci are
Staphylococci have several pathogenicity markers part of the autochthonous flora and are probably not the primary
including production of the clumping factor, hemolys- cause of this problem. This affected Amazon parrot belonged to a
ins, DNase, phosphatase, protein A and leuko- client who smoked, and when the owner started washing her hands
after smoking (presumably to remove nicotine sulfate, a potent
cidine. The presence of the clumping factor seems to toxin), the foot and leg lesions resolved. The client eventually
correlate closely with pathogenicity in avian pa- stopped smoking and the bird had no further episodes of Amazon
tients. Other pathogenicity markers have not been foot necrosis.
966
ods of time outside the host. Given proper conditions, Exogenous infections usually result in localized skin
the organism can propagate in an external environ- disease, although subsequent septicemia can occur in
ment. Like many bacteria, Staphylococcus can also some cases. Birds, unlike mammals, are generally
develop resistance to disinfectants following continu- resistant to wound infection. To become established,
ous exposure, and frequent changing of disinfectants exogenous bacteria typically require epithelium
is required to prevent the development of resistant damaged by other infectious agents (particularly
strains. clostridia or poxvirus), immunosuppression (includ-
ing immunosuppressive viruses such as retroviruses
Techniques for differentiating between avian and or reovirus), environmental stressors or prolonged
mammalian strains of S. aureus remain unsatisfac- application of an antibiotic.
tory. Evaluating the type of lesions caused by experi-
mental subcutaneous infection of S. aureus in birds Localized problems associated with Staphylococcus
may prove valuable in differentiating between avian spp. can also result from a delayed hypersensitivity
and mammalian strains. reaction. This type of response is considered to be one
of the major factors in treating staphylococcus-re-
Pathogenesis lated bumblefoot.
The importance of Staphylococcus infections in birds
is clinically underestimated. Individual strains may Clinical Disease and Pathology
cause clinical problems in one bird while being con- Staphylococcus can induce a wide range of clinical
sidered normal autochthonous flora in another. Lipo- and pathologic lesions, including high embryonic
teichoic acid, a major component of the staphylococ- mortality, yolk sac or umbilical inflammation, septi-
cal wall, is instrumental in the specific capacity of cemia, arthritis-synovitis, osteomyelitis, vesicular
this organism to bind to host cell receptors, particu- dermatitis, gangrenous dermatitis and bumblefoot.
larly in the respiratory system. Such binding is a
precondition for colonization and subsequent infec- Endogenous infections usually cause internal le-
tion. However, avirulent strains can also bind to the sions, while exogenous infections frequently result in
same receptors and may compete for receptor sites, dermatitis and bumblefoot. Staphylococcal lesions in
preventing colonization of virulent strains. This the umbilical region are typically either dry and
process is called “bacterial interference.” Suitable brownish or smudgy, reddish and edematous. Clini-
strains of Staphylococcus have been used as prophy- cal problems are most common in newly hatched
lactic tools, especially in poults. Some of these chicks (up to ten days of age), in which the yolk sac
apathogenic strains also produce bacteriocin, which in the body cavity is not absorbed normally, with
can inhibit the growth of a variety of bacteria. possible decomposition of its contents.
Although endogenous infections can be primary, they Staphylococcus septicemia may be characterized by
are frequently secondary to respiratory tract coloni- nonspecific clinical signs including lethargy, ano-
zation and progress to septicemia. If an infected bird rexia, a kyphotic posture, ruffled plumage and sud-
survives the acute septicemic stage of the disease, it den death. The acute occurrence of necrosis to the
will typically develop localized changes. Focal lesions distal digits or adnexa of the head and neck is sug-
occur as a result of thrombi formation in the arteri- gestive of a thrombi-inducing infection, which can be
oles and capillaries, which leads to ischemic necrosis. a sequela to staphylococcus septicemia. During the
Clinically, these necrotic areas are frequently local- initial phases of the ischemic process, the involved
ized at the tips of the extremities and in the skin. In digits may be swollen, congested and painful, and
addition, infarction can also cause necrotic lesions in many affected birds exhibit lameness. The acute on-
internal organs, particularly the liver and kidneys, set of tremors, opisthotonos and torticollis can often
which are more difficult to discern clinically. The be linked to staphylococcus-induced necrosis in the
central nervous system (CNS) is another site prone CNS. Gross lesions associated with staphylococcus
t o Staphylococcus-induced lesions. Postsepticemic septicemia include petechiae and ecchymoses of in-
development of arthritis, tenovaginitis, osteitis and ternal organs. Chronic infections may result in endo-
osteomyelitis followed by chronic skeletal changes carditis valvularis. Histologic changes vary with the
are considered together as one disease process (Fig- clinical course of disease but typically consist of a
ure 33.7). These problems usually occur after a four- heterophilic and granulomatous response.
to seven-day period of septicemia.
Arthritis-synovitis, characterized by the formation of
serofibrinous or fibrinous inflammation of the
967
CHAPTER 33 BACTERIA
FIG 33.7 Staphylococcus spp. can cause osteomyelitis either secondary to septicemia or following an injury that allows colonization of the
bone. Chronic osteomyelitis, as demonstrated in this radiograph, typically requires surgery to remove necrotic tissue and long-term
antibiotic therapy, preferably with clindamycin because of its high affinity to bone and bone marrow.
synovial membranes of tendon sheaths and articular rus (or other immunosuppressive agents) may be
bursae, is frequently noted with staphylococcal infec- involved in the disease process. Histologic evaluation
tions in gallinaceous species. Any joint may be in- of biopsy samples is required to confirm an underly-
volved but there appears to be a predilection for ing poxvirus.
colonization of the tarsal and metatarsal joints. Fol-
lowing antibiotic therapy, staphylococcus may be pre- Staphylococcus-induced gangrenous dermatitis is in-
sent in its unstable L-form, which is difficult to treat. itially recognized by the occurrence of subcutaneous
edema and hemorrhage followed by inflammation of
In immature birds with active growth plates, Staphy- the skin. Affected skin is typically blackish and
lococcus frequently localizes in the epiphyseal area smudgy and feather loss is common. Clostridium
with secondary invasion of the bone marrow, result- perfringens or another Clostridium sp. is a common
ing in osteomyelitis. Endogenous osteomyelitis is secondary invader. Both Staphylococcus and Clos-
considered to be impossible after consolidation of the tridium require a triggering factor (often damaged
growth plate.46 Infection of the growth plates often epithelium) to enter the tissue. Gangrenous derma-
leads to chronic skeletal abnormalities. Infections titis is rare in most bird species.
are frequently localized to the proximal epiphyses of
the femur, tibiotarsus, tarsometatarsus and fifth to Advanced bumblefoot is a necrotizing abscess on the
seventh thoracic vertebrae. Vertebral injury may plantar surface of the foot. Depending on the location
lead to clinical changes described as “kinky back” and chronicity of the abscess, infection may or may
(Figure 33.8). Swelling and colliquation associated not extend to neighboring joints, tendon sheaths and
with the infection cause deformation of the vertebral bones. The condition is frequently described in rap-
spongiosa, which may lead to narrowing of the verte- tors but may occur in other avian species. The precise
bral foramina and compression of the spinal cord. pathogenesis of bumblefoot is undetermined (see
Chapter 16). Although staphylococci are frequently
Staphylococcus-induced vesicular dermatitis is char- isolated from these lesions, they are by no means the
acterized by the formation of vesicles containing yel- only bacteria that can be recovered from diseased
lowish exudate that form brownish to blackish crusts tissue. Systemic infections that result in other le-
following rupture. Concomitant infection with poxvi-
968
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 infections
including Staphylococcus spp. can cause spinal deformities. In this bird, the WBC was normal and the etiology of the problem was
undetermined. Congenital abnormalities appear to be particularly common in African Grey Parrots and may have been the cause of this
scoliosis.
sions or death can occur secondary to bumblefoot dust and air), and some strains can survive for long
caused by virulent strains of S. aureus. periods in the environment. They are sensitive to
most commonly used disinfectants.
Diagnosis
Staphylococcal colonies, like Micrococcus spp., have Sc. and Ec. are considered part of the autochthonous
opaque pigments (from white to yellow). Clumping flora of the skin and the mucosal surfaces of the
factor-positive strains are likely to be virulent, and digestive, respiratory and reproductive tracts. Sc.
require an aggressive therapy based on antibiotic and Ec. transition from normal flora to disease-in-
sensitivities. ducing agents depends on the functional state of host
defense systems. Predisposing factors to disease in-
Serologic diagnostic techniques using agglutinins, clude immunosuppression, concomitant infections
antihemolysins or antitoxins are of little value in and exposure to a variety of toxins and pathogenicity
diagnosing staphylococcosis. Cross-agglutinins, par- factors that may be produced by some strains of Sc.
ticularly against Salmonella gallinarum-pullorum, and Ec.
frequently result in false-positive reactions.
The ß-hemolyzing, pyogenic streptococci, frequently
found in mammals, are rare in birds. In comparison,
Streptococcus (Sc.) and Enterococcus (Ec.)
α-hemolyzing streptococci are quite common. It has
Streptococci and enterococci consist of numerous spe- been suggested that most of the latter species should
cies that readily grow on most commonly used media. be included into the newly established genus Entero-
Differentiation between the species is based upon coccus.45,54 Enterococci are less fastidious than strep-
morphologic, biochemical and serologic charac- tococci, and many will grow on selective media used
teristics. These organisms are ubiquitous (mainly in for isolating Enterobacteriaceae. Numerous species
969
CHAPTER 33 BACTERIA
of streptococci and enterococci have

been isolated from birds.15,16,17,29
References to the pathogenicity of

several Sc. spp. vary. Variance in the
observed behavior of these opportun-
istic organisms may be a result of the
effects induced by concomitant viral
or chlamydial infections, the lack of
experimental infections and confu-
sion in taxonomy or nomenclature.
Irrespective of predisposing factors,
many Sc. and Ec. strains produce
compounds that facilitate an infec-
tion (M-protein, capsules) or produce
extracellular substances that inhibit
the host defense system (hemolysin
S, streptolysin S, hyaluronic acid,
streptokinase, DNase, NADase and
esterases) or inhibit other competing
bacteria (bacteriocins).
Vertical transmission (including L-

forms) can be a cause of early embryonic FIG 33.9 Bacterial infections (Streptococcus, Staphylococcus, Enterococcus and Salmo-
death and post-hatching develop- nella spp.) of the egg can cause embryonal death, post-hatching developmental problems
and yolk sacculitis.
mental problems (Figure 33.9). Infec-
tions in hatchlings are usually asso-
ciated with omphalogenic postnatal However, the pathogenicity of Ec. spp. is generally
septicemia. low. Experimental infections indicate that disease
induction requires predisposing immunosuppressive
Pathogenesis
factors. As a rule, natural infections occur by the oral
The rarely occurring Sc. spp. group C can cause a route and are most common in postnatal and growing
septicemia followed by an embolic-thrombotic sys- birds.
temic disease and death, usually in adult birds. Fol-
lowing infection, hematogenic and intrahepatic Ec. faecalis can induce an acute septicemic or a sub-
spreading results in colonization in almost all organs acute-chronic disease. The acute form predominates
if the host survives (probably agent- and host-spe- in young birds, and survivors often develop endo-
cific). In experimental infections, a persistent bac- carditis. Details on pathogenesis are known only in
teremia has been described, the duration of which gallinaceous species. Sc. faecalis is thought to play a
can range from weeks to months. In addition to the central role in the malabsorption syndrome de-
pathogenicity factors already mentioned, Sc. group C scribed in chickens.
may also produce reagins that govern the host reac-
tions. Genetic and environmental factors as well as Egg transmission of Ec. faecalis (also as an L-form)
concurrent viral infections or immunosuppressions is associated with an acute post-hatching septicemia.
may predispose mainly adult birds to this rare infec- The subclinically infected yolk sac is thought to be
tion. the source of disease in the hatchling. Ec. faecalis is
not considered autochthonous flora of canaries and
Little information is available on the pathogenesis of may cause a primary respiratory disease in this spe-
Sc. pneumoniae or Sc. pleomorphus lesions in birds. cies.18 Subacute-to-chronic tracheitis with dyspnea
Sc. bovis has been described as a pathogen in pi- and rales are considered natural components of the
geons17 and ducks;52 however, the pathogenesis of disease. Ec. cecorum has not been associated with
these infections is unclear. disease in experimental infections.14 Ec. columbae is
mainly found in pigeons and constitutes a component
Enterococci outside of the digestive tract can cause of the autochthonous intestinal flora.
necrotizing inflammatory lesions in infected organs.
970
Clinical Disease plete voice loss. Tracheal mites (Sternostoma tra-

The clinical diseases caused by pyogenic streptococci cheacolum) can cause similar clinical signs in this
and other streptococci and enterococci are relatively species. Epidemiologically, the infection spreads
similar. Clinical presentation can be peracute to slowly through the whole flock. Some affected birds
chronic, with birds surviving six to eight weeks in the develop dyspnea and die, while others may temporar-
chronic form. Omphalitis in recent hatchlings is typi- ily recover. Relapses are common in recovered birds.
cal with egg transmission or infections obtained from
the hatchery. Pathology
Gross lesions in birds that die acutely with bacter-
An Amazon parrot with a slight nasal discharge was emia include subepicardial and myocardial hemor-
found to have a Sc. group G infection that was caus- rhages and serofibrinous polyserositis. The subcuta-
ing chronic respiratory disease in the children of the neous tissues, serosal membranes and pericardium
house. Presumably, the bird was infected by the chil- may be congested, and the spleen is frequently hy-
dren. perplastic. Lung congestion, pneumonia or petechia-
tion of the laryngeal and tracheal mucosa may be
Septicemia may lead to a peracute apoplectiform noted in some species. The liver may be slightly
death or severe depression followed by death in two swollen and exhibit a greenish discoloration. Ca-
to three days. Other signs such as diarrhea, dyspnea, tarrhal enteritis, skeletal muscle hemorrhages and
paresis, conjunctivitis and sinusitis (Japanese Quail) swollen kidneys may also be observed. Muscle ne-
may develop. crosis and purulent myositis are frequently described
in pigeons with Sc. bovis infections.
Chronic disease is typified by inflammation of joints,
tendon sheaths and adnexa of the head. Fibrinous Pathologic changes in chronic cases are charac-
joint lesions, with or without abscess formation, can terized by arthritis with a light, mucoid exudate and
occur several months after the initial infection. Birds the formation of coagulated or dried exudates in the
that survive systemic infections may develop cardiac body cavity. Cauliflower-like or granulomatous
valve insufficiency secondary to endocarditis. This atrioventricular inflammation may develop, particu-
condition is difficult to diagnose and often presents larly on the left cardiac valve. Pyogenic streptococci
as chronic dyspnea. may cause chronic peritonitis, salpingitis and oo-
phoritis.
Sc. pyogenes has been associated with bacteremia in
the Humboldt Penguin, White Pelican, and several Histologically, focal necrosis is common in the liver.
Psittaciformes, Anatiformes and Phasianiformes. It This lesion is thought to be caused by bacterial endo-
has not been clearly defined whether the bacteremia toxins or the formation of thrombi in the bile ducts.
in these cases was a result of true group A strepto- Heterophilic infiltrates are most common in acute
cocci, or whether the inciting strain was Sc. pyogenes lesions. Granuloma formation (without a capsule and
animalis (classified in group C). Group C Streptococ- consisting of epithelioid cells and multinucleated gi-
cus has been associated with pneumonia secondary ant cells), particularly in the spleen and heart, is
to bacteremia in a variety of avian species. In the more common in chronic cases. Purulent meningitis
ostrich, Sc. group C cases are characterized by akine- has been described in some cases. Endocarditis and
sia, anorexia and dysphagia. This organism together cardiac infarct may occur secondary to embolic-
w i t h Corynebacterium pyogenes c a n i n d u c e thrombotic incidents. Localized lymph follicles may
diphtheroid lesions in the mucosa of the beak cavity be described as hyperplastic.
and the crop that can result in similar clinical signs.32
Diagnosis
Sc. bovis infections in pigeons have been associated In acute cases, samples for culture taken from the
with clinical changes ranging from peracute death to liver, heart and brain are most diagnostic. Isolation
chronic lameness (myositis) and arthritis. from the brain indicates that the strain recovered is
Ec. group D is frequently implicated as a cause of actively involved in the disease process. A triggering
pneumonia in various bird species, particularly Pas- factor might have been necessary to enable the or-
seriformes, and primarily infects young birds. In ca- ganism to cause septicemia. Special media are neces-
naries, Ec. faecalis can cause a tracheitis and chronic sary for culturing L-forms.
respiratory disease that manifests clinically as
changes in the voice (more “sparrow-like”) or com-
971
CHAPTER 33 BACTERIA
Mycobacterium (M.)
Colony morphology of pathogenic mycobacterium
may be smooth or rough and change through succes-
sive in vitro subcultures. Most strains are nonphoto-
chromogenic and may become yellow with age. Some
strains are scotochromogenic and have bright yellow
pigments.
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 in
infected 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 resistant
to environmental extremes and can survive in the
cage or aviary environment for periods ranging from
months to years. Shedding from an infected host
occurs primarily in the feces and urine, causing con-
tamination of the soil or water supplies within the
aviary. Mycobacterium has been found to remain
infectious in soil for up to seven years. For disinfec-
tion, only compounds tested against mycobacterium
are recommended.
M. avium and M. intracellulare: DNA cleavage

techniques (restriction fragment length polymor-
phism and pulsed-field gel electrophoresis) have
shown that M. avium consists of three clusters on the
subspecies level as follows:62
M. avium subsp. avium: This subspecies is ubiqui-

FIG 33.10 White streaking is evident in the pectoral musculature tous in the environment and is the agent most com-
of an Amazon parrot that was being treated with IM enrofloxacin.
monly associated with avian mycobacteriosis. The
organism also has a widely documented mammalian
Treatment and Control host range including cattle, sheep, goats, pigs, cats,
Aggressive treatment with parenterally adminis- kangaroos and humans. In humans, adults typically
tered antibiotics is the recommended therapy. Pyo- develop respiratory infections, children usually de-
genic streptococci are generally sensitive to penicil- velop submandibular adenopathies, and dissemi-
lins , eryt hromycin , ty los in, s pectinomycin, nated infections are common in patients with immu-
clindamycin and pleuromutilin. Enterococci have nosuppressive diseases (eg, AIDS). Strains
varying antimicrobial sensitivities. Chronic joint and experimentally caused paratuberculosis in cattle and
tendon sheath infections are difficult to resolve and tuberculosis in fowl (Table 33.5).
may require a combination of surgery, joint lavage
and prolonged antibiotic therapy. Joint lavage ap- M. avium subsp. paratuberculosis: This subspecies of
pears to be more successful in birds than in mam- M. avium requires mycobactin for in vitro culture
mals because iatrogenic secondary infections are less and has not been isolated from the environment. This
likely. Streptococci in synovial membranes are fre- subspecies is considered to cause paratuberculosis in
quently in their L- or protoplastic form. Treatment in ruminants and has been implicated as a cause of
these cases consists of ampicillin and erythromycin Crohn’s disease in humans.
or enrofloxacin (Figure 33.10).
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
972
isolated from Wood Pigeons and free-ranging rumi- Serovar 8 has been isolated worldwide and is prob-
nants. The agent causes paratuberculosis in mam- ably the most frequent serovar reported. Birds living
mals and mycobacteriosis as well as paratubercu- in aquatic environments are particularly susceptible
losis in birds. to infections, which can be subclinical. Recently, se-
rovars 25 and 27 have been isolated from sick birds.
M. intracellulare is designated as a distinct species In addition, M. avium strains have been recovered
and is considered less pathogenic to birds than M. that do not belong to serovars 1 to 28. These newly
avium (whether justified or not). Morphologic, bio- isolated strains vary serologically, have a broad host
chemical and serologic differentiation between M. spectrum and are considered as virulent as serovar 2.38
avium and M. intracellulare are relatively difficult.
These two species are routinely grouped together Transmission
into the M. avium-intracellulare (MAI) complex. MAI Avian mycobacteriosis primarily involves the alimen-
complex strains are serologically distinct and have tary tract. Transmission occurs mainly through con-
been divided into serovars.64 M. avium is divided into taminated feces, although aerogenic routes of trans-
serovars 1 to 11; M. intracellulare into three subspe- mission are possible. Arthropods can serve as
cies (subspecies 1: serovar 12 to 17, 19 to 28; subspe- mechanical vectors of M. intracellulare and M. avium
cies 2: serovar 7; subspecies 3: serovar 18). Serovar 1 subsp. avium. Egg transmission can occur but is
is most prevalent and pathogenic in the United epornitically unimportant because M. avium bacter-
States, while serovar 2 is most common in Europe. To emia causes an immediate cessation of egg produc-
date, serovar 3 has mainly been isolated in Europe. tion. Mycobacteria may persist in contaminated soil,
litter and, less frequently, feed. Birds of prey can be
secondarily infected while consuming infected
TABLE 33.5 Zoonotic Potential of Bacteria From Companion Birds quarry. The incidence of mycobacteriosis in free-
ranging birds is estimated to be less than 1%.59
Bacteria Zoonotic Potential
Actinobacillus None reported Pathogenesis
Alcaligenes None reported The main portal of entrance in birds is the intestinal
Bordetella None reported tract, which typically results in a visceral infection.
Campylobacter Undetermined, possible Initial colonization occurs in the intestinal wall. Sub-
C. laridis – diarrhea in children
clinical bacteremia occurs early with subsequent
Clostridium Negligible
spread to the liver through the portal circulation
E. coli Possible during the infectious process (relatively low numbers
Prevention – good hygiene
of organisms in the blood). The lack of lymph nodes
Erysipelothrix Persistent dermatitis
Avoid contact with infected birds allows unabated hematogenous spread within the
Haemophilus None reported host. The lungs can be secondarily infected during
Listeria Conjunctivitis when infected from birds bacteremia. Avian mycobacteria are removed from
Klebsiella Theoretically possible the endothelium of the vessels by reticuloendothelial
None reported cells, mainly in the liver, spleen and bone marrow.
Humans – Friedländers pneumonia Locally, avian mycobacteria induce cellular reactions
Megabacterium Avian-specific governed by the cell-mediated immune system. In
Mycobacterium Possible contrast to this typical M. avium infection, Columbi-
Immunosuppressed humans
formes, Anseriformes and some weaver finches of the
Pasteurella Rare human cases genus Textor develop lesions only within the lungs
Pseudomonas Possible (Figure 33.11). An acute bacteremia is frequently
Prevention – good hygiene
observed in cranes (Gruiformes), the Hermit Ibis,
Salmonella Negligible (see text)
Columbiformes and some Passeriformes. Tubercles
Staphylococcus aureus Negligible
Avian-adapted strains that form at the site of infection in the intestinal wall
Streptococcus/ Negligible commonly remain open to the intestinal lumen. This
Enterococcus Birds may be infected by humans allows for constant shedding of M. avium into the
Francisella tularensis Possible/unlikely from birds feces (open infection). In birds, three different types
Vibrio Mild enteritis of lesions can be recognized although the pathogene-
Yersinia High potential sis has not been clarified: 1) classical form with tu-
pseudotuberculosis Transmission documented bercules in many organs; 2) paratuberculous form
Humans – difficult to treat with typical lesions in the intestinal tract (prone to
973
CHAPTER 33 BACTERIA
ynx. In the Goshawk, loss of balance, convulsions and

necrosis of the base of the tongue have been ob-
served.43 Clinical signs associated with colonization
of the lung are rare. However, the peafowl may de-
velop respiratory sounds caused by granuloma for-
mation within the trachea.
Pathology
The pathology associated with M. avium infections
varies widely, probably based on the species of bird
infected and the serovar of the bacterium. Specific
relationships between avian hosts and individual se-
rovars have not been defined. The presence of miliary
to greater-than-pea-sized nodules in the wall of the
intestinal tract and in the liver, spleen and bone
FIG 33.11 In Psittaciformes, mycobacteriotic lesions are generally marrow are characteristic of M. avium infections.
not limited to the intestinal tract. In Columbiformes and some
other species, atypical granulomas may form in the lungs. Myco- These typical lesions have been described in Falconi-
bacterium avium was recovered from the lungs of this pigeon that formes, Accipitriformes, Strigiformes, Phasianifor-
was presented for severe emaciation and severe dyspnea. Radio- mes, Charadriiformes, Ciconiiformes, Cuculiformes,
graphs indicated soft tissue masses in the lungs. Abnormal clinical
pathology lesions included WBC=54,000 and PCV=19. Piciformes and Ralliformes. Granuloma formation
can occur in any organ but is generally localized to
the intestinal tract and reticuloendothelial organs.
develop this form of myobacteriosis are Amazona, The nodules are frequently necrotic in the center and
Pionus, Brotogeris, Psittacula species and the in chronic cases may be calcified. In contrast, Colum-
Horned Parakeet); 3) non-tuberculous form, which biformes, Anatiformes, Passeriformes and most of
may be difficult to recognize at necropsy (many Psit- the Psittaciformes do not form typical granulomas.
taciformes). Acid-fast rods are found distributed throughout the
parenchyma of infected organs. An infected liver or
Clinical Disease spleen may be only swollen or may show necrotic foci
In some bird species the clinical course is atypical, or even general induration. In pigeons, liver lesions
and acid-fast rods have been detected more or less may resemble Trichomonas abscesses. In pelicans,
accidentally. This is particularly the case with small greasy tumor-like swellings like those seen in leuk-
Passeriformes, especially the Hooded Siskin.19 Clini- osis may be observed. The lungs, particularly of
cal signs associated with mycobacteriosis are highly geese, weaver finches (genera Queleopsis, Quelea and
variable. Adult birds usually develop a chronic wast- Euplectes) and some Amazona spp., develop necrotiz-
ing disease associated with a good appetite, recurrent ing or ulcerating lesions. Paratuberculous lesions are
diarrhea, polyuria, anemia and dull plumage. Imma- characterized by the occurrence of clubbed villa con-
ture individuals frequently develop subclinical condi- taining acid-fast rods in the intestinal mucosa. Le-
tions. Intermittent switching lameness may occur as sions may also occur in glands of Lieberkühn, with
a result of painful lesions in the bone marrow. Arthri- characteristic proliferation of their epithelial cells.
tis, mainly of the carpometacarpal and the elbow
joints or tubercle formation of the muscles of the Histopathologic identification of foci of single or con-
thigh or shank can be seen occasionally. These clini- fluent epithelioid cells in affected organs is sugges-
cal changes are particularly common in Falconifor- tive of an M. avium infection. Parenchymal lesions
mes and Accipitriformes. Skin over the affected joint generally consist of epithelioid cells or multinu-
is often thickened and ulcerated. Tubercle formation cleated giant cells (mostly the foreign body type, only
in the skin is rare, but when it is present, pinpoint to rarely the Langhans type) and occasionally contain
pigeon egg-sized nodules filled with yellow fibrinous lymphocytes and plasma cells. Acid-fast rods in vary-
material may be noted. Granulomas may be seen ing quantities can be demonstrated in the affected
within the conjunctival sac, at the angle of the beak, epithelioid or multinucleated giant cells. Acid-fast
around the external auditory canal and in the oro- rods may also be noted in tissues in the absence of
pharynx. Mycobacteriosis should be suspected when cellular reactions. Some infected birds will have cell-
tumor-like lesions recur after surgery. Greater Rhea free acid-fast rods in the proventriculus or jejunal
frequently develop granulomas in the upper phar- villi without an inflammatory response. It has been
974
postulated that the acid-fast rods may actually be Several indirect tests have been discussed for diag-
contained within lymphatic vessels in the villi. M. nosing Mycobacterium. The tuberculin test (aller-
avium infections frequently induce depletion of lym- genic test) and the slide agglutination test (serologic
phocytes in the spleen (particularly the white pulp) test) have both been used in birds with some success.
and a proliferation of macrophage or reticular cell The tuberculin test is frequently associated with
types in the same tissue. Depletion of the splenic false-negative results, particularly in early and late
lymphocytes and lymph follicles may induce an im- stages of the disease and is no longer recommended.
munosuppression. The slide agglutination test requires fresh plasma or
serum and is evaluated against a bank of antigens for
Diagnosis the different serovars; there are cross-reactions be-
The demonstration of acid-fast rods in tissues or on tween the different serovars. Unfortunately, only se-
cytologic preparations is suggestive of mycobacte- rovar 2 antigen is commercially available. To esti-
riosis. False-negative staining can occur by not ob- mate the probability of an acute disease process,
taining an adequate sample. The demonstration of serotitration (using the Gruber-Widal scheme) is pos-
acid-fast rods in the feces has been suggested as a sible. Only titers greater than 1:64 are considered
useful diagnostic tool in subclinical birds. Mucus positive. Psittaciformes may exhibit a cyclic reduc-
present in the feces can interfere with test results, tion in titer and mycobacterial excretion, which may
and samples should be processed with one of the lead to an incorrect suspicion that natural healing or
sputum solvents used in human medicine before a successful therapy has occurred. An ELISA system
staining. The most consistent results can be obtained has been tested to distinguish between M. avium
by centrifuging the feces and then spreading the serovars but has been hampered by a high degree of
surface of the pellet on a slide for staining. This test cross-reactivity.
is relatively insensitive and requires the presence of
approximately 104 bacteria/g of feces to be positive. Treatment and Control
The clinician must differentiate between pathogenic Several treatment modalities have been discussed
and nonpathogenic strains of mycobacteria, both of for birds with M. avium infections. However, treating
which may be present in the feces. In general, non- infected birds is not recommended because:
pathogenic strains are wider and are not granular. All M. avium isolates that have been tested are
Demonstrating acid-fast organisms in the stool is not totally resistant to the antituberculous drugs rou-
diagnostic for a mycobacterial-induced disease. tinely used in humans. Recent information re-
vealed that ethambutol, while ineffective, does
Culture is required to make a distinct diagnosis.
change the cellular wall of M. avium in a manner
Some strains of M. avium-intracellulare require my-
that allows other tuberculostatics to enter the
cobactin and will not grow on egg medium. M. avium
organism.21 However, successful therapy is then
subsp. paratuberculosis and subsp. silvaticum can be
dependent on pharmacokinetic conditions and re-
separated by responses to six parameters: subsp.
quires a combination of drugs to be available at the
paratuberculosis has a mycobactin requirement,
same time, at the correct concentration and at the
grows on egg medium, tolerates cycloserine (50
correct anatomic location. The pharmacokinetic
µg/ml), is stimulated by pyruvate but not by pH 5.5,
data necessary to ensure that these parameters
and has no alkaline phosphatase. The subsp. silva-
are met are not available for a single avian species.
ticum has the opposite characteristics.62
M. avium infections are considered to be “open,”
Unfortunately, most of the mycobacterial strains allowing infected birds to continuously shed large
from Psittaciformes have not been cultured. The fu- numbers of organisms into the environment.
ture availability of species-specific antibodies will There is potential danger to man, and there is no
help in delineating infections. Endoscopy (with biop- appropriate method of treatment for infected hu-
sies) can be used for diagnosis in cases of advanced mans.
classical tuberculosis. Radiographs may indicate
granulomas in respiratory tissues in some cases. Birds that are definitively diagnosed (biopsy of af-
Biopsy is required to differentiate between mycobac- fected tissue with histopathology and culture) with
terial and fungal granulomas, which radiographi- M. avium or M. intracellulare infection should be
cally appear similar. euthanatized. Contact birds should be removed from
the contaminated area, quarantined for two years
and tested every six to 12 weeks to determine if they
975
CHAPTER 33 BACTERIA
are reacting. Birds that remain negative (also not Pathogenesis

shedding the agent with the feces) and are in good E. rhusiopathiae infections are most common in wa-
physical condition following the quarantine proce- terfowl and fish-eating birds during cold weather
dure can be considered free of the disease. There are when food is scarce and energy requirements are
currently no absolute means of control. The chances high. Concomitant infections and inadequate hy-
of introducing M. avium-positive birds to the flock giene seem to be precipitating factors of natural dis-
can be reduced by performing serologic or repeated eases. Most affected birds die during the bacteremic
fecal examinations of all new additions during the phase of an infection. Those birds that survive the
quarantine period. acute disease frequently have secondary dermatitis
and arthritis caused by hypersensitivity reactions.
The transmission of M. avium to humans is possible.
However, transmission is probably dependent on in- Clinical Disease and Pathology
herent resistance, the immune status of the person E. rhusiopathiae usually causes peracute death. If
in question, the frequency of exposure and the num- clinical signs occur, they may include lethargy, weak-
ber of bacteria per exposure. ness, anorexia and hyperemia or bruising of the
M. tuberculosis: M. tuberculosis lesions in Psittaci- featherless, nonpigmented skin. Greenish discolored
formes are possible but are extremely rare. When droppings, dyspnea and nasal discharge have been
present, they are generally characterized by the for- reported in some cases. In the Marabou Stork, infec-
mation of benign localized granulomas of the dermis, tions have been characterized by inflammation and
frequently around the cere or nares as well as the necrosis of the cutaneous adnexa of the neck.
retroorbital tissue.63 Birds affected are usually pets Petechiae in the subcutis, musculature and intesti-
with very close human contact and, as such, serve as nal mucosa are common gross lesions in diseased
sentinels for patent tuberculosis in the owners. The birds. The liver and spleen are friable and discolored
affected dermis looks granulomatous and may even (red to black). Histologically, these organs are degen-
ulcerate. The swelling of the retrobulbar tissue erated and necrotic. Chronic E. rhusiopathiae cases
causes a protrusion of the eye (exophthalmos). Diag- are rare but have been reported in geese and turkeys.
nosis can be made by histology or culture of biopsies. Clinical changes associated with this form of disease
Infected birds should be euthanatized. include thickened, leather-like skin, serofibrinous
M. bovis: M. bovis was associated with a generalized arthritis or valvular endocarditis. Histologic changes
infection in an Amazon parrot. This animal developed in these tissues include thrombi and degeneration of
a nontubercular lesion similar to those seen in Psit- vascular walls.
taciformes infected with M. avium intracellulare. The
Diagnosis
strain in question was sensitive to all common tuber-
Diagnosis is confirmed by isolating E. rhusiopathiae.
culostatic drugs.
The best samples for isolation (if the tissues are
fresh) are liver or spleen. In severely autolytic cases,
Erysipelothrix (E.) bone marrow samples may be the most diagnostic. As
in most bacterial diseases, cell-mediated immunity is
Erysipelothrix rhusiopathiae can induce an acute-to-
more important in resolving infections than the de-
subacute septicemic disease. Infections are most
velopment of humoral antibodies. Thus, serologic
commonly discussed in ducks and geese but can occa-
methods of diagnosis are of little value.
sionally occur in other avian species including Psit-
taciformes.55,32 The eleven serotypes of E. rhusiopa- E. rhusiopathiae adjuvanted bacterins have been
thiae are ubiquitous in the environment and can used to control flock outbreaks; however, vaccination
propagate outside the host. Survivability in moist may sensitize the birds and potentiate chronic dis-
soil and in the water of shallow lakes and ponds, even ease. Flock control can best be implemented through
salt and seawater, is particularly high. Infections in sound aviary hygiene and rodent control.
birds occur most frequently in the late fall, winter
and early spring (northern hemisphere). Rodents,
pigs and raw fish have all been implicated as reser- Listeria (L.)
voirs for the bacterium. Listeria monocytogenes causes β-hemolysis on blood
agar. The motility of listeria is dependent on the
ambient temperature to which it is exposed. Listeria
976
spp. may infect a number of avian

species, 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 in
areas. The bacteria is environmen-
tally stable and can propagate out-
side the host.56
Pathogenesis
The role of L. monocytogenes as a
primary pathogen is controversial;
however, there is no question that
ingested bacteria can lead to a latent
or abortive infection. Acute disease is
characterized by bacteremia pro-
gressing to death within one to two
days. The subacute and chronic
forms of the disease involve reactions FIG 33.12 Encephalitis caused by several bacterial pathogens including E. coli, Listeria,
of the cell-mediated immune system. Salmonella, Staphylococcus and Klebsiella spp. can cause neurologic signs characterized
by torticollis, tremor, ataxia, depression, paresis or paralysis.
Intracellular bacteria like L. monocy-
togenes typically induce cell-medi-
ated immunity.
samples. Listeria isolates must be speciated, because
L. ivanovii, L. innocua and L. seeligeri are commonly
Clinical Disease and Pathology recovered from birds.8 There is little information on
Clinical disease is usually associated with sporadic the pathogenicity of these Listeria spp. although L.
deaths in a collection. Epornitics can develop in ca- innocua is considered apathogenic.37 Latent infec-
naries and related birds that are maintained in tions limit the diagnostic value of serologic tests
dense populations. Chronic infections can induce le- (slide agglutination).
sions in the heart, liver and, rarely, the brain. If
clinical signs are noted, they are generally associated
with CNS signs and include blindness, torticollis, Clostridium (Cl.)
tremor, stupor and paresis or paralysis (Figure The genus Clostridium includes a group of ubiqui-
33.12).41 Subacute-to-chronic cases usually cause a tous bacteria that are considered to be
severe monocytosis (10 to 12 times normal). autochthonous flora in raptors and in birds with well
developed ceca, including Phasianiformes (gallina-
The presence of serofibrinous pericarditis and myo-
ceous birds) and Anseriformes. In birds in which the
cardial necrosis is considered suggestive of Listeria.
cecum is small or absent, clostridium is rarely iso-
There are usually no gross lesions evident in the
lated from the intestinal tract and when it is, it is
brain. There may be no lesions in birds that die
often considered to be transitory.
acutely, or there can be a few petechiae present.
Histologically, infections are characterized by degen- Pathogenesis

erative lesions, without a cellular response, in the Clostridium spp. produce more potent toxins than
heart and liver. Brain tissue is usually normal, even any other bacterial genus. The pathogenesis of Cl.
in cases in which CNS signs are present and the spp. toxin-induced damage in a bird remains poorly
organism can be recovered from the cerebrum. understood except for Cl. botulinum. This Cl. sp.
principally causes an alimentary intoxication. The
Diagnosis ability of clostridia to colonize the intestines appears
A confirmed diagnosis requires the isolation of L. to depend on reduced gastrointestinal motility. Peri-
monocytogenes from affected tissues. Appropriate staltic abnormalities can occur as a result of enteri-
transport media are necessary for proper shipment of tis, low levels of dietary fiber, administration of some
977
CHAPTER 33 BACTERIA
medications, or during some viral infections (particu- The differential diagnosis includes salmonellosis, en-
larly reovirus). Experimental reproduction of disease terotoxic E. coli and drug overdoses. Newcastle dis-
by using a culture alone is usually not possible, and ease virus can induce ulcers called “boutons” that
clostridial organisms are considered to be opportun- resemble those induced by Clostridium.
istic pathogens. Following colonization, pathogenic
clostridia produce exotoxins, which then induce clini- Gangrenous Dermatitis
cal lesions or death. Gangrenous dermatitis can be caused by Cl. perfrin-
gens type A, Cl. septicum, or Cl. novyi. These organ-
It is best to discuss clostridial infections by grouping isms can directly colonize damaged skin. Microscopic
them under clinical signs because a clostridial spe- epithelial lesions caused by abrasions, avipoxvirus or
cies can cause differing clinical signs, and various staphylococci can become secondarily infected with
clostridial species can cause similar-appearing dis- Clostridium spp. The patient’s immune status may
eases. also play a role in the overall pathogenesis.
Necrotic or Ulcerative Enteritis The sudden occurrence of regional feather loss with
Clostridia-induced enteritis can occur in many avian a blue-red or almost black skin discoloration is a
species. Flock outbreaks are most commonly associ- characteristic lesion. Affected skin may also be ede-
ated with Phasianiformes, especially those within matous and painful as a result of gas accumulation
the subfamilies Tetraoninae (grouse) and Odonto- in the tissue. Sick animals typically develop toxemia
phorinae (New World quail) or captive and free-rang- and die within 24 hours. With screamers (genus
ing lorikeets.44 Ulcerative gastritis, not enteritis, is Chauna), their corneous-lined bony wing spurs can
the most common form of clostridial infection re- cause prick-like skin injuries predisposing them to
ported in the ostrich.60 Clostridial enteritis in game clostridial diseases.
birds (Tetraoninae) is usually associated with Cl.
perfringens type A. On rare occasions, types B, C or The occurrence of emphysema, edema and hemor-
D may be the etiologic agent. Cl. perfringens type E rhages (with or without necrosis) in the subcutis,
is vary rare in Phasianiformes. Ulcerative enteritis skeletal musculature and myocardium are charac-
in the Bobwhite Quail is usually caused by Cl. teristic necropsy findings. A confirmed diagnosis re-
colinum (species incertae sedis). This organism is quires isolation of Cl. spp. from affected tissues.
also thought to cause necrotic enteritis in the other Aeromonas hydrophila, s t a p h y l o c o c c i a n d
Odontophorinae, grouse, chicken, turkey and domes- avipoxvirus can induce pathologic changes similar to
ticated pigeon (Köhler, personal communication). those caused by Cl. spp. Rapid production and sys-
temic release of toxins usually prevents successful
Necrotic enteritis usually occurs in young birds after therapy.
the second post-hatching week. Adult birds are more
resistant. In the acute form of the disease, clinical Botulism (syn. Limberneck)
changes include diarrhea (with or without blood) and
polydipsia, followed by death within a few hours. Cl. botulinum neurotoxins are typically ingested in
Birds with chronic lesions exhibit retarded growth contaminated foods. Rarely, clinical disease may re-
and weight loss before dying. sult from primary colonization of the alimentary
tract. Cl. botulinum has been found to produce six
Pathologic changes include diffuse or focal hypere- thermolabile exotoxins (designated A to F). Types A
mia of the mucosa, which develops into necrotic areas and C are predominantly involved in inducing
or ulcers. These lesions are most common in the pathologic changes (occasionally also type E). High
upper jejunum. Lesions start as pinpoint foci and concentrations of clostridium toxins are common in
progress to include a necrotic center with a wall and decaying meat and vegetation. Fly larvae (maggots)
a reddish halo. Ulcers may coalesce and perforate the that feed on decaying material are resistant to the
intestinal wall. Swelling and necrosis of a grayish toxins but can serve as a source of intoxication for
liver, spleen and kidney are common. those species that eat maggots. With a few logical
exceptions, most birds are probably susceptible to Cl.
Identification of characteristic lesions and isolation
botulinum toxins. Free-ranging waterfowl are par-
of the organism are confirmatory. If Cl. perfringens is
ticularly susceptible, and enzootic intoxications are
the etiologic agent, a diagnosis can be achieved by
common following periods of drought or flooding.
demonstrating toxins in the serum, intestinal con-
Vultures seem to be resistant to the toxins (by a still
tents and liver homogenates (sterilized by filtration).
978
unknown mechanism), and some raptors (that eat Tetanus

carrion) have a reduced susceptibility.
A few cases of Cl. tetani intoxication in birds have
Foods contaminated with Cl. botulinum toxins have been reported in older literature. There have been no
no particular change in taste or smell and are thus cases of tetanus reported in birds using more confir-
difficult to detect. Toxins enter the body through the matory diagnostic tests. Generally, birds are consid-
intestinal wall, move to the ends of the autonomic ered to be highly resistant to Cl. tetani; cases re-
and somatic efferent nerves and then ascend into the ported in older literature may have been incorrectly
spinal cord. Once in the spinal cord, toxins selectively diagnosed.
and irreversibly bind to the neuromuscular junctions
and block the production of acetylcholine. Death is Other Gram-positive Rods
due to respiratory paralysis. Toxins also damage vas-
cular endothelium, resulting in edema and petechia- Bacillus spp., Corynebacterium spp., Streptomyces
tion. spp. and Lactobacillus spp. are commonly recovered
from avian-derived samples. Because these organ-
Flaccid paralysis of the skeletal musculature (includ- isms are frequently isolated from clinically normal
ing the tongue) is the characteristic clinical change. birds, they are considered to be components of the
Bulbar paralysis, feather loss and diarrhea may be autochthonous flora. Megabacterium is considered to
noted in some birds. Birds with substantial clinical be a pathogenic organism, although little informa-
signs usually die, although a few can spontaneously tion is currently available on its involvement in avian
recover. Recovery is more likely with type A rather disease. Bacillus spp. isolated from birds are difficult
than type C toxin. Petechial hemorrhage of the cere- to differentiate, and most have not been described
bellum and focal necrosis and hemorrhage of the taxonomically. Bacillus anthracis has not been asso-
central lobe of the cerebrum are indicative of Cl. ciated with clinical disease in birds, presumably be-
botulinum, but there are no pathognomonic lesions. cause their high body temperature inhibits the pro-
duction of the pathogenic toxins. Vultures, and to a
Confirming a diagnosis requires using mouse animal
lesser extent raptors, are known to be mechanical
models to demonstrate the presence of toxins in se-
vectors.
rum, filtered liver or kidney from an affected animal.
Feed or water (sewage, mud) extracts from a pond None of the Corynebacterium (Co.) spp. that have
also provide diagnostic samples. Cl. botulinum tox- been isolated from birds have been found to be patho-
ins are heat-sensitive and degrade at room tempera- genic. Ostriches have been reported to have concomi-
ture. Materials to be tested should be preserved by tant Co. pyogenes and Sc. group C infections.32 Anti-
deep-freezing (-20°C). bodies to Corynebacterium spp. and Mycobacterium
avium-intracellulare can cross-react, making differ-
Intoxication with some algae, eg, red tide (see Chap-
entiation between these organisms difficult.
ter 46), may cause clinical signs similar to those
caused by Cl. botulinum. Affected birds usually have Streptomyces spp. can occasionally be isolated from
access to muddy, drying bodies of water. Aeromonas the avian respiratory system. The pathogenicity of
hydrophila can cause the acute death of large num- the organism is questionable. Some reports describe
bers of waterfowl that consume contaminated water. nocardia in birds. These cases were described based
A rapid death, typically in the summer, is charac- on bacterial morphology and not on analysis of wall
teristic, but some infected birds can develop signs components, which is necessary to confirm nocardia
that mimic those of Cl. sp. toxin ingestion. A. hydro- in infected tissues.
phila and Cl. botulinum may both cause epornitics of
acute death in connection with contaminated water. Lactobacillus spp. can be identified on the mucosa of
the intestinal, respiratory and reproductive tracts of
Flock problems can be prevented by reducing contact many avian species. In birds that do not possess
with decaying foods, removing cadavers, providing Enterobacteriaceae as a normal component of the gut
toxin-free feed (especially for insect eaters) and regu- flora, lactobacillus seems to play an important role in
lating the water level and temperature in waterfowl inhibiting colonization of Enterobacteriaceae (al-
collections (see Chapter 46). A commercial type C though probably not in many species of grouse). Sup-
antitoxin is available for mink and has proven to be plementing with lactobacillus has been discussed as
effective in birds. One-half of the dose recommended a method of inducing a natural competitive inhibition
for mink should be used in birds.
979
CHAPTER 33 BACTERIA
TABLE 33.6 Survey of Clinically Important Bacteria
Bacteria Characteristics Incubation Transmission Disinfectants/Stability

Alcaligenes/ Motile Turkeys – 5-7 days Alc. ingestion Resistant to drying
Bordetella 0.3-0.5 x 1-2 µm Others – unknown Shed in feces Environmentally stable
Egg transmission (Particularly low temps)
Bord. respiratory tract, feces
Egg transmission
Campylobacter Gram-negative 5 to 15 days Ingestion Survives 1 week out of host
Motile rod Feces Most disinfectants effective
0.2-0.5 x 1.5-5 µm
Clostridium Gram-negative Experimental – hrs to 3 days Ingestion Resistant in environment
Anaerobic Natural – unknown Wound infection Spores – survive years
Spore-forming rod Most disinfectants ineffective
Autoclaving/flaming effective
Erysipelothrix Gram-positive Turkeys, ducks – 1.8 days Ingestion Most disinfectants effective
Nonmotile rods Other birds – unknown Egg transmission (stork)
0.2-0.4 x 1-2.5 µm
E. coli Gram-negative Experimental – 24 to 48 hrs Ingestion – mainly Most disinfectants effective
0.5 x 3 µm Aerogenic – dust
Motile or nonmotile rod Egg transmission
(normal & L-forms)
Haemophilus Gram-negative H. paragallinarum Respiratory tract Survives a few days
0.3-0.6 x 1-3 µm 1-5 days Asymptomatic carriers Most disinfectants effective
Coccoid-to-pleomorphic rods
Listeria Gram-positive Unknown Ingestion Most disinfectants effective
0.4 x 0.5-2 µm Common in aquatic
Motile rod environments
Reptiles, amphibians, snails
natural reservoirs
Mycobacterium Gram-positive Weeks to years Feces, urine Persists in contaminated
Acid-fast Exposure and immune system Aerogenic possible (rare) soil or litter for years
Granulated short-to-long rods dictate Arthropods-mechanical vectors
Pasteurella Gram-negative Vary with species Upper respiratory tract Not stable to stable
Nonmotile Cat bite – 6-48 hrs Fecal shedding rare depending on conditions
Ovoid-to-coccoid rod See text Most disinfectants effective
Pseudomonas Gram-negative Specifics unknown Ingestion Pseudo: resistant to most
Aeromonas 1-3 x 0.3-0.6 µm Pseud — few hrs Proliferates in H20 disinfectants – steam,
Aero — 1-3 days Secondary in open wounds boiling H20 effective
Aero: most disinfectants
effective
Salmonella Gram-negative Varies with type Ingestion Dried feces stable – 8 months
0.5 x 3 µm Acute 3-5 days Egg transmission to 2 years
Motile, rarely nonmotile Egg — 2 days Normal and L-forms Water stable – 3 weeks
rod Most disinfectants effective
>60°C kills most strains
Staphylococcus Gram-positive Unknown Vertical, horizontal Environmentally stable
0.8 x 1.0 µm Few hrs to few months Normal & L-forms Most disinfectants ineffective
Nonmotile Latent infections Chronic carriers
Spherical coccoid
Streptococcus Gram-positive <2 µm Mammals – days to weeks Horizontal, vertical Probably no growth in
Enterococcus Coccoid-to-ovoid pairs or Birds – unknown Shed in feces environment
chains Aerogenic Sc spp – short-lived
Percutaneous (skin lesion) Ec spp – long-lived
Yersinia 0.4 - 0.8 x 0.8 - 1 µm Days to 2-3 weeks Ingestion Most disinfectants effective
Motile or nonmotile Carrier birds & rodents
Ovoid-to-coccoid rods Direct contact
Fecal contaminated food or
water
980
TABLE 33.7 Bacterial Control and Therapeutics
Bacteria Treatment/Control Bacteria Treatment/Control

Actinobacillus Tetracyclines/chloramphenicol Klebsiella Resistant to many antibiotics
See text Rx based on sensitivity
Enrofloxacin initially
Aeromonas Most antibiotics
See text Listeria Tetracyclines
CNS signs – poor prognosis
Alcaligenes/Bordetella Antibiotic resistance common
Hygiene critical
Rx based on sensitivities
Megabacterium No effective therapy
Borrelia Tylosin/Spectinomycin
Resistant to all tested antibiotics
Control ticks
Control – unknown
Strain-specific vaccines
Acidifying water with HCl
Campylobacter Erythromycin/tetracyclines
Mycobacterium Not recommended
Streptomycin, non-psittacines
See text
Furane derivatives in non-waterfowl
(See text) Pasteurella Parenteral antibiotics
See text
Clostridium perfringens Clindamycin/spiramycin
Control –
Laxatives – Remove unabsorbed toxins
Prevent rodents/free-ranging birds
Wound irrigation
Vaccines – poor efficacy
Control – Vaccination (toxoid)
Zinc bacitracin (200 ppm) Pseudomonas Resistant to many antibiotics
(Bobwhite Quail in food) Rx based on sensitivity
Prevent skin wounds Enrofloxacin initially
Systemic infections usually fatal
Clostridium botulinum Toxoid vaccine, antitoxin
See text
Laxatives – remove unabsorbed toxins
Guanidine – (15 to 30 mg/kg) Salmonella See text
May bind neurotoxin Staphyloccocus Resistant to many antibiotics
Prevent food contamination Semisynthetic penicillins pending
Activated charcoal sensitivity
See text Bumblefoot – Debride, antibiotics
Cytophaga Parenteral antibiotics Heparin – prevents fibrin
Treat soon after hatching Streptococcus Parenteral antibiotics
Bacterins provide sero-specific Enterococcus See text
protection Control – hygiene
Escherichia coli Rx based on sensitivity Stimulates minimal immune response
See text Yersinia See text
Erysipelothrix Parenteral penicillin/doxycycline
Surgically remove affected skin Treatment of all bacterial infections should be based on specific
Hyperimmune serum antibiotic sensitivity. Supportive care in the form of fluids and enteral
See text feeding is frequently necessary. Correcting predisposing factors that
Haemophilus Most antibiotics cause immunosuppression in the host or allow exposure to an organ-
Sulfonamides – drug of choice ism are critical control methods. Preventing exposure to rodents,
Sinusitis – surgical drainage insects and free-ranging birds can reduce bacterial exposure. Hygiene
Flushing is always important, particularly in neonates, to prevent reinfection.
Topical vitamin A
Asymptomatic carriers
Detect by culturing sinuses
Polyvalent vaccine – poor efficacy
of gram-negative and other pathogenic bacteria. How- Isolation of megabacteria is difficult, and biochemi-
ever, there are strong indications that many groups of cal descriptions that would allow appropriate taxo-
birds have specific lactobacilli that can effectively colo- nomic classification have not been performed. This
nize the gut. Strains derived from soured milk do not organism has a unique morphology and is a large (1
colonize the avian gut and must be given daily for two x 90 µm) gram-positive rod.13 Successful culture re-
to four weeks in order to lower the gastrointestinal quires the use of Merck’s MRS medium; however, not
tract pH. This drop in pH will favor the colonization of all megabacterial strains have been found to grow on
autochthonous microorganisms. Inhibitory expulsion this medium. The colonies are rough and measure 3
itself takes from four to six weeks, provided no serious to 4 millimeters in diameter with a dented margin.
triggering factors interfere.23 Development requires 48 hours in a moist chamber.
Subcultures are progressively more difficult and the
organism may stop growing in successive passages.28
FIG 33.13 A group of budgerigars was presented for occasional
melena and chronic weight loss over a prolonged period. Large (1
x 90 µm) gram-positive rods (suggestive of megabacteria) could be
detected in the feces. Radiographs in various affected birds indi-
cated a,b) proventricular dilatation and c,d) filling defects and
ulceration in the proventriculus. At necropsy, the filling defects
were found to be globules of mucin that had a propensity to
accumulate at the isthmus. It should be noted that the presence of
a dilated proventriculus is not diagnostic for neuropathic gastric
dilatation (courtesy of Nina Ungerechts).
982
TABLE 33.8 Differential Diagnoses of Bacterial Infections
Arthritis or Synovitis Enteritis Cytophaga (duck septicemia)

Staphyloccoccus E. coli Pasteurella spp.
Actinobacillus sp. Aeromonas sp. Haemophilus
E. coli Most enteric organisms Chlamydiosis (eg, psittacines,
E. rhusopathiae (ducks and goose) Pseudomonas spp. Columbiformes)
Mycobacterium avium Salmonella spp. Salmonella spp.
Mycoplasma spp. E. rhusiopathiae Septicemia
Pasteurella multocida Chlamydiosis E. coli
Salmonella spp. Listeria sp. Many bacteria
CNS Signs Pasteurella spp. Listeria spp.
Listeriosis Hepatitis E. rhusiopathiae
Chlamydiosis Most bacteria that cause septicemia Pasteurella spp.
E. coli Campylobacter Salmonella spp.
Klebsiella pneumoniae Pasteurella spp. Yersinia pseudotuberculosis
Listeria monocytogenes Chlamydiosis Pseudomonas/Aeromonas
Salmonella spp. Salmonella spp. Most Enterobacteriacae
Dermatitis Pseudomonas enteritis Staphylococcus (mimics numerous
Pseudomonas/Aeromonas spp. Clostridium spp. other infectious agents)
Clostridium spp. Streptococcus/Enterococcus
Respiratory Disease Borrelliosis (high tick areas)
Staphylococcus spp. Alicalgenes
Enterobacteriaceae
Pasteurella spp.
Morphologically similar strains of megabacterium involve intermittent periods of recovery. Severely af-
that were considered normal components of the fected birds may pass digested blood in the feces.
budgerigar proventricular flora have been de- Contrast radiography typically indicates a sand-
scribed.53 glass-like retraction between the proventriculus and
ventriculus (Figure 33.13). This finding is considered
Some researchers believe that megabacterium is the highly suggestive of megabacteriosis.31 Megabac-
causative agent of progressive weight loss (“going terium is shed in the feces and can be detected by
light syndrome”) in budgerigars. The name “going gram-stained samples from severely sick birds.
light syndrome” should provisionally be replaced by
megabacteriosis, because weight loss is a clinical At necropsy, a proventriculitis or proventricular ul-
sign of a variety of chronic diseases. Experimental cer with or without hemorrhages can be observed.
infections with pure cultures of megabacterium in- Lesions are most common in the pars intermedia
duce disease only in English standard budgerigars gastris. The organisms lie densely together in the
and not in the normal breed.28 These findings suggest necrotic tissue foci. There is usually little inflamma-
that birds vary in susceptibility to the organism, and tory cellular reaction associated with the organism,
other factors are involved in the pathogenesis. Spon- which can be seen readily at low magnification from
taneous recovery was common in experimental cases. proventricular scrapings. Impression smears from
The host spectrum includes canaries34 and related the liver and spleen may be useful in detecting the
finches, cockatiels, lovebirds, chickens and young bacteria, which can be encapsulated in the tissues.
(3-week-old) ostriches (Hüchzermeier, unpublished). There is no treatment because of resistance to all
antibiotics commonly used.
Clinically infected birds develop chronic emaciation
over a 12- to 18-month period that may or may not
983
CHAPTER 33 BACTERIA
References and Suggested Reading

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teurella multocida in soil and water finches. Proc Assoc Avian Vet, 1983, 36.Karmali MA, et al: Taxonomy of the 52.Rinaldi, et al: Episodi di streptococ-
in an area where avian cholera is en- p 62. genus Campylobacter. In Butzler PJ cosi dell’anatra. Atti della Societa
zootic. J Wildl Dis 22:257-259, 1986. 20.Dorrestein GM, et al: Campylobacter (Hrsg) (ed): Campylobacter infection Italiana della Scienze Veterinarie
3.Bergey’s Manual of Systematic Bacteriol- infections in cage birds: clinical, in man and animal. Boca Raton, CRC 24:665-666, 1970.
ogy: Vol 1. Baltimore, London, Los pathological and bacteriological as- Press Inc, 1984, pp 1-20. 53.Scanlan CM, et al: Characterization
Angeles, Sydney, William and pects. Proc Joint Meeting Vet Pathol, 37.Knorz W, et al: Zur Pathogenität von of a gram-positive bacterium from
Wilkins, 1984. Utrecht, 1984. Listerien. Immune Infect 14:76-80, the proventriculus of budgerigars
4.Bisgaard M, et al: Isolation, charac- 21.Dortbudak, et al: In vitro activity of 1986. (Melopsittacus undulatus). Avian Dis
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of Vibrio cholera NAG isolated from 12th Conf Europ Soc Mycobac, Pra- riose durch bisher nicht identifizier- 54.Schleifer KH: Transfer of Streptococ-
Danish duck farm. Avian Pathol gue, 1991. bare Stämme. J Vet Med B 38:3-10, cus faecalis and Streptococcus
19:271-276, 1975. 22.Dwars FG, et al: Incidence of spiroche- 1991. faecium to the genus Enterococcus
5.Böttger EC: Systematik, Differ- tal infections in cases of intestinal 39.Koppers N, et al: Mykobakteriose bei nom. rev. as Enterococcus faecalis
enzierung und Nachweis von bakter- disorder in chickens. Avian Pathol Waldrappen (Geronticus eremita). comb. nov. and Enterococcus faecium
iellen Infektionserregern - die Fami- 18:591-595, 1989. Berl Münch Tierärztl Wschr 104:57- comb. nov. Int J Syst Bacteriol 43:31-
lie Mycobacteriaceae. Immun Inf 23.Eichinger E: Lactobacillen zur 62, 1991. 34, 1984.
19:143-152, 1991. Bekämpfung von Enterobacteriaceen 40.Korbel R: Epizootiologie, Klinik und 55.Schröder H-D: Beitrag zu den Infek-
6.Braumiller W: Zur Charakterisierung im Darm von Psittaciformes. DVG Therapie der Pasteurella- multocida- tionskrankheiten der Zoo- und Wild-
von Hämolysinen aus aviären Aero- VII. Tagung Vogelkrankheiten, Infektion beim Vogelpatienten nach vögel. IV. DVG-Tagung Vogelkrht,
monas-hydrophila-Stämmen. Vet München, 1990, pp 231-234. Katzenbiß. Tierärztl Prax 18:365- München, 1985, pp 173-174.
Dis, München, 1991. 24.Forster F, et al: Mycobacteria in psit- 376, 1990. 56.Sinn LC: Listeriosis in birds. Proc As-
7.Bredy JP, et al: The effects of six envi- taciformes. Proc 1st Intl Conf Zool & 41.Korbel R: Ocular manifestations of soc Avian Vet, 1988, pp 189-190.
ronmental variables on Pasteurella Avian Med 39-56, 1987. systemic diseases in birds. Proc 57.Skirrow MB: Campylobacter enteri-
multocida populations in water. J 25.Gerlach H: Diagnose der Pseudotu- Europ Assoc Avian Vet, 1991, pp 157- tis: A “new” disease. Br Med J 2:9-11,
Wildl Dis 25:232-239, 1989. berkulose bei lebenden Vögeln. DVG- 167. 1977.
8.Bühler-Nickel E: Untersuchungen Tagung Krankht. der Vögel, 42.Lauwers S et al: Campylobacter sero- 58.Small PJ: Spirochetosis on a Califor-
zum Isolierungsverfahren, Vorkom- München, 1979, pp 96-101. typing and epidemiology. Lancet 158- nia pheasant ranch: A case report.
men und zur Differenzierung von Lis- 26.Gerlach H: Infection with the so- 159, 1981. Proc 33rd West Poult Dis Conf, 1984,
terien beim Geflügel. DVG-Tagung called Haemophilus septicaemia an- 43.Lumeij JT, et al: Observations on tu- p 31-33.
Fachgruppe Bakteriologie, 1990, pp seris in geese. Proc VIIth Intl Cong berculosis in raptors. In Cooper JE, 59.Smit EK, et al: Avian tuberculosis in
74-86. WVPA, 1981, p 80. Greenwood A (eds): Recent Advances wild birds in the Netherlands. J Wild-
9.Calnek BW, et al (ed): Diseases of 27.Gerlach H: Bacterial diseases. In Har- in the Study of Raptor Diseases. life Dis 23:485-487, 1987.
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ated with Pasteurella anatipestifer in- delphia, London, WB Saunders Co, 44.McOrist S, Keece RL: Clostridial en- Poult Dis Conf, 1991, pp 258-260.
fection in turkeys. Proc 41th West 1986, p 434. teritis in free-living lorikeets, (Tricho- 61.Stoll L: Kälteanreicherung von
Poult Dis Conf, 1991, p 54. 28.Gerlach H: Going light in budgeri- glossus spp.). Avian Pathol 21:503- Yersinia pseudotuberculosis zum
11.Crosta L, et al: Oral treatment with gars. Proc Assoc Avian Vet, 1986, pp 507, 1992. Nachweis aus Untersuchungsmate-
clindamycin in racing pigeons. Proc 247-250. 45.Mundt JO: Enterococci. In: Bergey’s rial. (Vortrag, 1966) ref Zbl Hyg Bakt
Euro Assoc Avian Vet, 1991, pp 293- 29.Gratzl-Köhler: Spezielle Pathologie Manual of Systematic Bacteriology I ref 206:534, 1967.
296. und Therapie der Geflügelkrank- Vol 2, Baltimore, London, Los Ange- 62.Thorel M-F, et al: Numerical taxon-
12.Davelaar FG, et al: Infectious typhli- heiten. Stuttgart, Ferdinand Enke les, Sydney, Williams and Wilkins, omy of mycobactin-dependent myco-
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cientific principles of bacteriology are uni-

S versal; however, in application, bacteria can

Example of Bacterial Taxonomy: BACTERIA

Bacterial infections may be primary or secondary.

autochthonous flora is considered normal, and only

TABLE 33.2 Birds in which Enterobacteriaceae are not normal Pathogenesis

Most vertebrates can be infected

Incubation periods vary with the type of salmonella

infection. Presumably, these differences are depend-

geese and ducks. Some infected

Subgenus III strains are considered

Postmortem lesions include dehydra-

freundii antibodies often cross-react with those to S.

Citrobacter spp. cause serious secondary infections in

Treatment Both of these bacteria infect many mammals, includ-

C. jejuni may appear in different forms including a

common histologic finding. Catarrhal enteritis (also Transmission

produced by Pasteurella damage blood vessels, caus-

Clinical Disease and Pathology

Postmortem findings with acute disease may be ab-

of streptococci and enterococci have

References to the pathogenicity of

Vertical transmission (including L-

Clinical Disease plete voice loss. Tracheal mites (Sternostoma tra-

All bird species that have been experimentally ex-

M. avium and M. intracellulare: DNA cleavage

M. avium subsp. avium: This subspecies is ubiqui-

ynx. In the Goshawk, loss of balance, convulsions and

are reacting. Birds that remain negative (also not Pathogenesis

spp. may infect a number of avian

L. monocytogenes is a ubiquitous or-

Histologically, infections are characterized by degen- Pathogenesis

unknown mechanism), and some raptors (that eat Tetanus

TABLE 33.6 Survey of Clinically Important Bacteria

Bacteria Characteristics Incubation Transmission Disinfectants/Stability

TABLE 33.7 Bacterial Control and Therapeutics

Bacteria Treatment/Control Bacteria Treatment/Control

TABLE 33.8 Differential Diagnoses of Bacterial Infections

Arthritis or Synovitis Enteritis Cytophaga (duck septicemia)

References and Suggested Reading

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