Bacterial Diseases of Wildlife

• 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

Depression, anorexia, ataxia, roughened coat, tendency to huddle.

Sheep - susceptible 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.

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.

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

TularemiaTransmission 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 well-defined 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

– 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 38-40C. 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

BrucellosisTransmission 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.

LymeTransmission and

Epidemiology• Natural reservoir –

white-footed mouse• Vector – ticks in the

genus Ixodes

LymeNymph

Adult

EggsEggs

Larva

LymePathologyDeposited in skin by ticks during

feedingReplicate in dermis for ~ 1wkDisseminate to distant cutaneous

sites, organs, jointsLocalized 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.

AnthraxTransmission 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.

AnthraxComplicated “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.

AnthraxComplicated “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.

AnthraxPathology• 3 routes of entry

1. Gastrointestinal – across intact mucous membranes or defects in epithelium of oropharynx or GI

2. Cutaneous – spores enter through cuts and abrasions

3. 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

– 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• Mycobacterium bovis• Gram positive, rods• Acid-fast• Phylum Acintobacter• Aerobic

Bovine TB

Pathogenic features• Intracellular in macrophages

– Prevent phagosome-lysosome fusion

Bovine TBTransmission 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 TBTransmission 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 TBTransmission 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 TBSymptoms• 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 TBPathology• tiny droplets containing

1-3 bacteria reach the alveoli (10-200 droplets)

• phagocytized by un-activated alveolar macrophages

• M. bovis survive– impair normal phagocyte

functions– multiply

• young phagocytes are actively recruited but don’t kill

Bovine TBPathology• local infection• spread via lymphatics to

regional nodes• then thru blood to any

other organ– spread to CNS, spongy

bone, liver, kidney, genitals

• host immune response usually kills infected macrophages and halts infection

Bovine TBPathology• 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 TBPathology• 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.

• 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.