Bacterial Diseases of Wildlife
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Tularemia
Brucellosis
Lyme borreliosis
Anthrax
Bovine Tuberculosis
Tularemia – aka rabbit fever
Basic Micro
• Francisella tularensis
• Gram negative
• Phylum Proteobacteria
Class Gamma
• Obligate aerobic
• Non-spore-forming
• 4 known subspecies
– Type A – more virulent – N. America
– Type B – less virulent - Europe
In liver cells
Animal
Clinical Signs
Lagomorphs – very
susceptible
Depression, anorexia, ataxia, roughened coat,
tendency to huddle, weakness, fever, ulcers,
abscesses at site of infection, swelling of regional
lymph nodes, sudden death caused by septicemia.
Rodents – very
susceptible
Sheep - susceptible
Depression, anorexia, ataxia, roughened coat,
tendency to huddle.
Dogs – fairly resistant
Low fever, mucopurulent ocular and nasal discharge,
abscesses at site of infection, axillary and inguinal
vesiculopapular rash, loss of appetite, listlessness,
lymphadenopathy, anorexia.
Humans
Fever, localized skin or mucous membrane
ulceration,
regional lymphadenopathy, and, occasionally,
pneumonia.
Sudden onset of fever, lethargy, anorexia, stiffness,
reduced mobility, signs of septicemia, depression,
dysnpnea, diarrhea, lag behind rest of the herd,
coughing, pollakiuria, abortions, carry heads high
when walking, weak or rapid pulse, frequent
urination, death.
Tularemia
Pathogenic features
• Pili (attachment to host tissue)
• Capsule (protects against complement)
• Facultative intracellular (cytoplasm of host
macrophages)
• AcpA – acid phosphatase, inhibits respiratory
burst (avoid destruction by phagocytes)
• Siderophore (small molecules that bind iron,
then taken up by bacterium)
• 30 kb pathogenicity island – iglC (escape),
pdpD, pdpA - unknown
Tularemia
Transmission and Epidemiology
• Can persist for long periods of time in moist environs
(water, mud, decaying animal carcasses).
• Reservoirs
– Natural - small and medium-sized mammals
• North America – leporidae, castoridae, muridae, sciuridae
– Natural - Acanthamoeba
– Incidental - humans, other mammalian species, some species of
birds, fish, and amphibians.
• Vectors
– Hard ticks – primary vector of Type A - transovarian
– Biting flies
– Mosquitoes
Tularemia
Pathology
• Infection – dose,10 cells
• To regional lymph nodes
– Engulfed by macrophages
– Escape from phagosome into
cytoplasm within 3-4 hours
Lymph nodes show welldefined zones of
necrosis, predominantly
in the outer cortex.
100X
400X
Tularemia
Pathology
• Hematogenic dissemination to liver, spleen, lungs
The most common
pulmonary histologic
finding is suppurative
pneumonia with
areas of necrosis
and hemorrhage.
Sections of liver
showed rounded
microabscesses.
Tularemia
Pathology
• Typical lesions are pale white
to gray, often slightly raised
necrotic foci, ranging in size
from pin-point to a few
millimeters in diameter.
• Impairment of organ functions
(liver, spleen, lungs)
• Death in susceptible – 2-10
days
Brucellosis – aka Malta fever,
Bang’s disease, undulant fever
Basic Micro
• Brucella
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B. abortus (cattle)
B. melitensis (goats)
B. suis (swine)
B. ovis (sheep)
B. canis (dogs)
• Gram negative
• Phylum Proteobacteria
Class alpha
• Aerobe
• Non-spore-forming
Animal
Clinical Signs
Domestic,
feral, wild
Abortion, retained placenta,
enlarged testicles, pendulous
scrotum
Humans
Acute febrile disease - fever 3840C. Unusually severe limb and
back pain, sweating and fatigue are
marked. On physical examination,
splenomegaly may be the only
finding. Untreated, symptoms may
continue for 2 - 4 weeks.
Persistent disease - arthritis, often
sacroiliitis, and spondylitis (in about
10% of cases), CNS effects
including meningitis (in about 5%).
Brucellosis
Pathogenic features
• Lacks “classical” virulence
factors
• Facultative intracellular in
monocyte-macrophages
• Cell-wall polysacc protects cell
from phagosome and inhibits
apoptosis
• Escapes phagosome, replicates
in ER
• Enterobactin (iron chelator)
• Stimulates polyclonal B cell
activation
entering a macrophage
massive proliferation in macrophage
Brucellosis
Transmission and Epidemiology
• Transmitted via ingestion of contaminated feed, licking
infected fetus, calf, placenta; also conjunctival, inhalation
• Reservoirs
– various wild, feral and (particularly) domestic animals. In ruminants,
enormous numbers of bacteria are shed widely from infected
products of conception, whether aborted or born at term. Brucellae
frequently invade the mammary gland of infected ruminants.
• Individuals are infected for life, and herds are chronically
infected
Brucellosis
Pathology
• Invades from point of entry
• Bacteremia + entry into phagocytes
• Initial localization in regional lymph
nodes and spleen.
• Invasion of reproductive organs
• Severe inflammation of the placenta
prevents oxygen and nutrient
delivery to fetus and removal of
waste products  fetal death
• Alternately – hormonal dysregulation
results in premature delivery.
Lyme
Most prevalent tick-borne
disease of humans in
US – 20,000/yr
Basic Micro
• Borrelia burgdorferi
• Gram negative
• Spirochete
Lyme
Pathogenic features
• Erp outer membrane lipoproteins (protect from
complement-mediated killing)
• One of the few pathogens that does not require iron.
• Different genes expressed in tick vs mammal.
Lyme
Transmission and
Epidemiology
• Natural reservoir –
white-footed mouse
• Vector – ticks in the
genus Ixodes
Lyme
Nymph
Eggs
Eggs
Larva
Adult
Lyme
Pathology
Deposited in skin by ticks during
feeding
Replicate in dermis for ~ 1wk
Disseminate to distant cutaneous
sites, organs, joints
Localized inflammatory response
triggered by surface antigens
w/ unusual prod. of interleukin
and interferon
Anthrax
One of oldest diseases known –
account in the book of Exodus
Basic Micro
• Bacillus anthracis
• Gram positive
• Phylum Firmicutes
Class Bacilli
• Obligate aerobe
• Spore-forming
Anthrax
Pathogenic features
• Capsule
• Toxin complex consisting of:
– Cell-receptor binding protein called protective antigen
– Two separate toxins
• Edema factor (EF)
• Lethal factor (LF)
• Toxin complex works to:
– prevent apoptosis
– increase capillary permeability
– reduce blood clotting
Anthrax
• Symptoms that may appear immediately
before death are high temperatures,
bloody discharge, and swelling in the neck
and shoulder areas.
• Carcasses – dark blood, not clotting.
Bloody serous discharges from nose, etc.
Anthrax
Transmission and Epidemiology
• Persistence depends on extreme virulence, death of the host, and
survival of highly resistant spores in the environment for prolonged
periods.
• Infects a wide range of homeothermic species (body temp is critical).
• Carcasses of dead
animals attract
scavengers that free
vegetative cells and
disperse them over a wide area.
• Herbivores are much
more susceptible than
carnivores – but
carnivores and
scavengers are carriers
of spores, transmitted in feces.
Anthrax
Complicated “life cycle”
• Vegetative B. anthracis require aerobic and high nutrient
conditions.
• When host dies, tissues become anaerobic.
• B. anthracis are held in stasis, unable to replicate or
sporulate
• Anaerobic bacteria
from GI, esp.
Clostridium spp.
decompose carcass.
• Carcass is opened
and vegetative
B.
anthracis dispersed.
Anthrax
Complicated “life cycle”.
• In the environment, low nutrient
conditions and dehydration
stimulate sporulation.
• Spores resistant to extremes of
temp., UV, desiccation,
chemicals…
• Epidemics tend to occur in moist
lowland areas where soil is high
in organic content, in dry
summer months following period
of heavy rain or floods – role of
water.
Anthrax
Pathology
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3 routes of entry
1.
2.
3.
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Gastrointestinal – across intact mucous
membranes or defects in epithelium of
oropharynx or GI
Cutaneous – spores enter through cuts
and abrasions
Inhalational – spores inhaled to alveoli
of lungs
Spores germinate into
vegetative cells
Carried to lymph nodes
Anthrax
Pathology
• Cross into bloodstream and
disseminate via circulation
• Terminal blood concentration
greater than 107 CFU/mL.
• Produce toxins
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Edema
Shock
Acute renal failure
Terminal anoxia
Death
In bovine blood
Bovine tuberculosis
Mycobacterium bovis is the causative agent of
tuberculosis in a range of animal species and
man, with worldwide annual losses to agriculture
of $3 billion.
Basic Micro
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Mycobacterium bovis
Gram positive, rods
Acid-fast
Phylum Acintobacter
Aerobic
Bovine TB
Pathogenic features
• Intracellular in macrophages
– Prevent phagosome-lysosome fusion
Bovine TB
Transmission and Epidemiology
• M. bovis can be transmitted by the inhalation of
aerosols, by ingestion, or through breaks in the
skin. The importance of these routes varies
between species.
• Bovine tuberculosis is usually maintained in
cattle populations, but a few other species can
become reservoir hosts. Most species are
considered to be spillover hosts.
Bovine TB
Transmission and Epidemiology
• Natural, primary host – cattle
• Maintenance hosts - brush–tailed opossums (and
possibly ferrets) in New Zealand, badgers in the United
Kingdom and Ireland, bison and elk in Canada, and kudu
and African buffalo in southern Africa. White-tail deer in
MI and MN.
• Spillover - sheep, goats, horses, pigs, dogs, cats, ferrets,
camels, llamas, many species of wild ruminants
including deer and elk; elephants, rhinoceroses, foxes,
coyotes, mink, primates, opossums, otters, seals, sea
lions, hares, raccoons, bears, warthogs, large cats
(including lions, tigers, leopards, cheetahs and lynx) and
several species of rodents.
• Most mammals may be susceptible.
Bovine TB
Transmission and Epidemiology
• Cattle shed M. bovis in respiratory secretions, feces and
milk, and sometimes in the urine, vaginal secretions or
semen. Large numbers of organisms may be shed in the
late stages of infection.
• Some animals become infected when they ingest the
organism; this route may be particularly important in
calves that nurse from infected cow.
Bovine TB
• The symptoms of bovine tuberculosis usually take
months to develop in cattle. Infections can also remain
dormant for years and reactivate during periods of
stress or in old age.
• Similarly, severe disease can develop in some deer
within a few months of infection, while other deer do
not become symptomatic for years.
Bovine TB
Symptoms
• Tuberculosis is a chronic, progressive disease that can
cause gradual debilitation and is manifest as emaciation,
depression, and intolerance to exercise.
• Because infection often involves the lungs, coughing,
nasal discharges, and difficulty breathing can occur in
severe cases.
• In some instances, superficial lymph nodes in the neck
will develop large abscesses that may rupture and drain
through the skin.
Bovine TB
Pathology
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tiny droplets containing
1-3 bacteria reach the
alveoli (10-200 droplets)
phagocytized by unactivated alveolar
macrophages
M. bovis survive
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impair normal phagocyte
functions
multiply
young phagocytes are
actively recruited but
don’t kill
Bovine TB
Pathology
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local infection
spread via lymphatics to
regional nodes
then thru blood to any
other organ
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spread to CNS, spongy
bone, liver, kidney,
genitals
host immune response
usually kills infected
macrophages and halts
infection
Bovine TB
Pathology
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At necropsy, tuberculosis
lesions are variable in
appearance and size.
Subclinically infected
animals may have one
or a few small necrotic
nodules that usually are
associated with the
lymph nodes of the head
and neck or the lungs.
Bovine TB
Pathology
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More severely infected cervids can
have multiple pea-sized nodules or
large cheesy or pus-filled masses in
the same areas. The classical
tubercle, which is firm, white or pale
yellow, and gritty when cut, does
occur in cervids, but many M. bovis
lesions in these animals are filled
with pus.
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In cervids, tuberculous lesions are
most often seen in the lymph nodes
of the head and neck or in lung
tissue; however, lesions can occur
throughout the chest cavity, under
the skin of the chest, and in the
abdominal cavity as well.