Bacterial Diseases of Wildlife Tularemia Brucellosis Lyme borreliosis Anthrax Bovine Tuberculosis

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Text of Bacterial Diseases of Wildlife Tularemia Brucellosis Lyme borreliosis Anthrax Bovine Tuberculosis

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  • Bacterial Diseases of Wildlife Tularemia Brucellosis Lyme borreliosis Anthrax Bovine Tuberculosis
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  • 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
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  • AnimalClinical 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.
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  • 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
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  • 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
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  • Tularemia Pathology Infection dose,10 cells To regional lymph nodes Engulfed by macrophages Escape from phagosome into cytoplasm within 3-4 hours
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  • Lymph nodes show well- defined zones of necrosis, predominantly in the outer cortex. 100X 400X
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  • Tularemia Pathology Hematogenic dissemination to liver, spleen, lungs
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  • The most common pulmonary histologic finding is suppurative pneumonia with areas of necrosis and hemorrhage.
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  • Sections of liver showed rounded microabscesses.
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  • 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
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  • Brucellosis aka Malta fever, Bangs 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
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  • AnimalClinical 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%).
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  • 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
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  • 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
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  • 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.
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  • Lyme Most prevalent tick-borne disease of humans in US 20,000/yr Basic Micro Borrelia burgdorferi Gram negative Spirochete
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  • 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.
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  • Lyme Transmission and Epidemiology Natural reservoir white-footed mouse Vector ticks in the genus Ixodes
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  • Lyme Nymph Adult Eggs Larva
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  • 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
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  • 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
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  • 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
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  • 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.
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  • 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.
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  • 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.
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  • 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.
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  • Anthrax Pathology 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
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  • Anthrax Pathology Cross into bloodstream and disseminate via circulation Terminal blood concentration greater than 10 7 CFU/mL. Produce toxins Edema Shock Acute renal failure Terminal anoxia Death In bovine blood
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  • 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
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  • Bovine TB Pathogenic features Intracellular in macrophages Prevent phagosome-lysosome fusion
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  • 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.
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  • Bovine