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69 Cards in this Set

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Mycobacterium Spp.
 Gram positive rods
 Lipid-rich thick cell wall  Acid-fast
Resistant to antibiotics Resistant to environmental factors
Cell wall – adjuvant
Mycobacterium Spp.
General Characteristics
 Atmospheric – Obligate/strict aerobic
 Location – Facultative/obligate intracellular  Habitat – Carriers, water, sewage, soil
 Transmission – Inhalation, ingestion, contact
Mycobacterium Virulence Factors Surface Virulence Factors
 Mycolic acids
 Trehalose dimycolate (cord factor)
 Lipoarabinomannan (LAM)
 Sulfolipids
TB complex
Tuberculosis
M. avium complex
Avian tuberculosis Swine mycobacteriosis
M. avium ssp paratuberculosis
Ruminant Johnes
M. lepraemurium
Cat leprosy
Mycobacterium Spp. – Disease
 TB complex M. bovis
M. tuberculosis
 Bovine/Ruminants /Swine/Avian/Others
Bovine Tuberculosis
 Clinical signs
Weight loss,
Cough, fever, & nodules
 Occur in a small number of infected animals
Bovine Tuberculosis
Diagnosis
Skin test – tuberculin test
PPD = purified protein derivative
 INF-γ test
Laboratory identification (BSL-3)  Acid-fast stain/PCR
 Culture (special medium)
Bovine Tuberculosis
Control/Prevention/Treatment
 Test-and-slaughter
 Notify state/federal authorities  Control wildlife
 No vaccine/no treatment
Mycobacterium avium Complex (MAC)
M. avium – ubiquitous, many serovars
Avian tuberculosis – granulomatous lesions in
free-range adult birds
Swine mycobacteriosis – granulomatous lesions in lymph nodes
Bovine exposure – complicates TB/Johne’s diagnosis
M. avium subsp. paratuberculsis (MAP) – Johne’s Disease
 MAP = slow growth (4 mo).
 Mycobactin J-dependent for growth
 Neonates and calves – susceptible
 Long incubation time (2-5 yrs)
 Clinical signs – weight loss/diarrhea (4 to 7 yrs)  Chronic granulomatous lesion in intestine
Johne’s Disease – Clinical Signs
 Weight loss
 Diarrhea (late)
 Intestinal Necrosis (late)
Johne’s Disease
Transmission/Diagnosis/Prevention
 Fecal-oral route  Serology (ELISA)
 Fecal culture/PCR
Herold’s egg yolk agar (16 wks) Radiometric culture (4 wks)
 Reduce environmental contamination  No vaccine/no treatment
Feline Leprosy
M. lepraemurium
 Obligate intracellular –
No culture
 Granulomatous skin lesions
 Transmitted by rat bite
Nontuberculous Mycobacteria
Opportunistic Infections
M. marinum
M. fortuitum
Nontuberculous Mycobacteria
Diagnosis/Treatment
Clinical signs Acid-fast stain
Laboratory culture (>7 days)
Antibiotic treatment: Trimethoprim- sulfa, Doxycycline
Mycobacterium spp -zoonosis
 TB complex – Yes
 Avium complex – Yes Immunocompromised individuals
 Fast growers – Yes Immunocompromised individuals
 MAP – Crone’s disease?
Rhodococcus equi
General Characteristics
 Gram positive coccobacilli
 Capsule
Rhodococcus equi
General Characteristics
Atmospheric – Obligate aerobic Location – Facultative intracellular Habitat – Soil saprophytes
Transmission – Inhalation, ingestion, contact
Rhodococcus equi
Pathogenesis
Surface Virulence Factors
 Virulence associated protein A (VapA) - Intracellular survival
Rhodococcus equi
Diseases
Foal pneumonia
Coincides with low maternal
Ab/low GI flora
High dose-exposure Suppurative colitis
Swine lymphadenitis Granulomatous lesion Carcass condemnation
Opportunistic infections Many Species & Humans
Rhodococcus equi
Diagnosis
Laboratory culture: Trans-tracheal aspirate
Abscess material
 Treatment
Passive immunoprophylaxis
 Antibiotics: Erythromycin/rifampin
Rhodcoccus equi – Zoonosis
Yes, immunocompromised individual
Haemophilus felis
Rhinitis & conjunctivitis in cats
Third most significant organism in conjunctivitis in cats
Chlamydophila felis Mycoplasma spp.
Haemophilus paragallinarum
Infectious coryza
Upper respiratory disease of chickens Different serogroups and strains
Fowl cholera (Avian cholera)
P. multocida (capsule type A)
Highly contagious fomites, water, new birds excretions contain bacteria
septicemia
Swollen wattles, joints, foot pads, Conjunctivitis, respiratory signs
P. multocida
Fowl cholera Highly contagious septicemia
H. Paragallinarum
Infectious coryza
Upper respiratory tract infection
Taylorella equigenitalis
Gram and shape
negative
rod or coccobacilli (pleomorphic)
Habitat
Genital tracts of horses Stallions - urethral fossa Mares – clitoral fossa
Atmospheric
Facultative anaerobic
Diseases
Contagious equine metritis
Transmission
During coitus
Special
REPORTABLE
Pasteurella multocida
5 serogroups
A,B,D,E,F
hemagglutination of capsular antigens
Eleven (11) somatic serotypes (1-11)
Types related to host specificity & pathogenicity (related to disease)
Pasteurella multocida
5 serogroups
A,B,D,E,F
hemagglutination of capsular antigens
Pasteurella multocida
serotypes B:2 (Asia) and E:2 (Africa)
Haemorrhagic septicemia Not present in the USA
Foreign Animal Disease
Haemorrhagic septicemia
Pasteurella multocida
serotypes B:2 (Asia) and E:2 (Africa)
Pasteurella spp
Virulence factors Capsule
- may facilitate adherence to surfaces
- interfere with phagocytosis and protects
from complement system attack complexes
- different capsular serotypes have different chemical makeup which are similar to that of host tissue
- reduces the antigenicity of the capsule
fimbria
- may facilitate adherence to surfaces
- expression of adhesins can be due to environmental cues
- different strains may possess different types of fimbriae, each with specificity for a particular receptor
lipopolysaccharide (LPS)
Endotoxin
toxic to respiratory epithelial cells decreases phagocytosis
elicits inflammatory reaction
Pasteurella multocida
Virulence factor - exotoxins Pmt (P. multocida toxin)
in P. multocida capsule type D
Pmt is osteolytic and induces bone resorption
Bacteria inhabits mucous membranes of the upper respiratory tract
Atrophic Rhinitis
P. multocida and Bordetella bronchiseptica
Initial infection with Bordetella bronchiseptica
If P. multocida not present, then get a mild, reversible turbinate hypoplasia
But,
B. bronchiseptica dermonecrotic toxin damages epithelial cells
allows P. multocida to adhere
www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=pmd &part=A1380&rendertype=figure&id=A1390
Pmt induces destruction and atrophy of nasal turbinate bones
Mannheimia spp
Virulence factors
Leukotoxin (Lkt) LPS
Capsule Fimbriae
] together drive a tissue destroying
inflammatory response
Adh1 (adhesin 1) Fibrinogen-binding proteins Other exotoxins
Bovine respiratory disease complex bronchopneumonia
fibrinous pleuropneumonia
Mannheimia haemolytica Pasteurella multocida
Bovine respiratory disease complex
Transmission
inhalation
Ingestion
Direct inoculation (bites, scratches, licking)
source is carrier or sick animals
Endogenous
- decreased host defenses allow commensal bacteria living in the upper respiratory tract to infect the lungs
Bovine respiratory disease complex
Diagnostics
Culture
strain typing
PCR
Samples
Nasopharyngeal & tracheal swabs Transtracheal aspirate Bronchoalveolar lavage
Lung aspirate
Transport media Anaerobic bacteria?
Pasteurella and Mannheimia spp
Prevention and control
elimination of reservoirs of pathogen reduce predisposing factors vaccination - not yet
Pasteurella and Mannheimia spp
Public health significance
P. multocida from bite wounds
Haemophilus
Gram and shape
negative
rod or coccobacilli (pleomorphic)
Habitat
Commensals of the mucosa of the oropharynx and GI tract
Do not survival outside host
Atmospheric
Facultative anaerobic
Diseases
H. paragallinarum
infectious coryza
H. felis
Rhinitis & conjunctivitis in cats
H. parasuis
Glässer's diseases
Transmission
Shed from nasal cavity
Inhalation, direct contact, ingestion of contaminated feed
Isolate infected animals virulent to non-virulent strains
Haemophilus parasuis
polyserositis (Glässer’s disease)
septicemia
VERY LITTLE IS KNOWN
Virulence factors: Capsules-15 types
Gram-negative cell wall LPS and endotoxin
Iron acquisition
Histophilus somni
(previously Haemophilus somnus)
along w/ M. haemolytica and P. multocida,
H. somni can be part of the Bovine respiratory
disease complex (Bovine shipping fever complex)
Thromboembolic Meningoencephalitis (TEME)
Disseminated multifocal hemorrhages and infarctions in spinal cord brainstem and cerebral cortex
Vasculitis – septic infarction and abscessation
Adheres to vascular endothelium – apoptosis and lysis of cells
Exposes subendothelial collagen –
initiates blood-clotting cascade and thrombosis
Histophilus somni – no capsule
Gain entrance into circulatory system
Septicemia
Histophilus somni
Diagnostics
Culture
Interpretation and sample site location
H. parasuis –
Normal flora Good sites
from freshly deceased pigs or (ideally) acutely ill pigs that are sacrificed.
peracute - disease case are lung, joint and brain
acute and chronic form - peritoneal fluid, fibrin in the peritoneum, lung and pericardial fluid.
Serology
Histophilus somni (AGGL) at TVMDL Infectious coryza
PCR (Infectious coryza)
Specimen requirements: Throat swab or sinus swab.
Brucella spp.
• Member of the family Brucellaceae
• Gram negative coccobacilli – Non‐motile
– Increased CO2
– Non‐spore forming
• Obligate pathogen
– Reproductive tract
– Reticuloendothelial system
• Atmospheric – Obligate Aerobe
• Location – Facultative Intracellular
• Environment – Can persist in the environment: – for up to 6 months at 0°C
– up to 125 days in dust or soil – up to 1 year in feces
• Transmission – Direct contact, Ingestion, Inhalation
Brucella spp.
Virulence Factors
• Surface Virulence Factors
– No capsules, spores, or flagella
– Lipopolysaccharide (LPS)
– Inhibits phagolysosome fusion • Prevents macrophage apoptosis
– Iron Acquisition
• Secreted Virulence Factors – Type IV secretion system
Brucella spp.
Species Affected
• Brucellaabortus
– Cattle
• Brucellasuis
– Bison – Elk
– Camels – Yak
– Pigs
• Cattle
• Caribou
• Brucellacanis
• Brucellamelitensis – Goats
– Dogs
• Brucellaovis
– Sheep – Camels – Alpacas – Llamas
– Sheep
• Brucellaneotomae
– Wood rat (Neotoma lepida)
• Brucellacetaceae
• Brucellapinnepediae
Reservoirs for the Brucella Species
• Brucellaabortus cattle
• Brucellamelitensis sheep/goat
• Brucellasuis pig
• Brucellacanis dog
• Brucellaovis sheep
• Brucella neotomae mouse
Brucella
Pathogenesis
• Enter/invade in the ileal Peyer’s patches
• Ingested
• Engulfed by macrophages
– Survive in the macrophage
• Suppress the myeloperoxidase H2O2 system
– Inhibit phagolysosome fusion in neutrophils
• Migrate to the lymph nodes where they infect other cells or are killed
• From lymph nodes, the Brucella disseminate – Reticuloendothelial system
– Reproductive tract
• In a pregnant animal, the Brucella infect the placenta and fetus
– Erythritol
– Localizes to the trophoblasts of the placentome – Spreads to the fetus
Brucella
Transmission
• Major source of infection – Aborted fetus
– Placenta
– Post abortion uterine fluids – Sexually transmitted
– Milk—calves, kids, humans – Urine—B. canis
Brucella
Survival Environment
• Survive for up to 4 months in milk, urine, water and damp soil.
– Moisture
– Temperature—cooler better
• Pasteurization effectively kills Brucella sp.
Brucellosis Testing
• Gold Standard—bacterial culture
• Serology
– Slide Agglutination • with rivanol
• with beta‐mercapthoethanol
– AGID (Agar Gel Immunodiffusion) – ELISA
– CFT (Complement Fixation Test)
– Fluorescence polarization
Brucellosis Vaccination
• B. abortus (cattle) – Strain 19
– RB51
• Cattle
– Calves less than 1 year of age
– Permanently identified • Ear tattoo
• Tamper proof ear tag
Brucellosis
Public Health Significance
• Veterinariansandabattoirworkers
• Labacquiredinfection
• Ingestionofunpasteurizeddairyproducts
Clinical Signs Human Brucellosis
• Chronicdebilitatinginfections
– Flu‐like symptoms...but much, much worse • Fever—undulant fever
• Night Sweats
• Fatigue
• Joint Pain (arthralgia and arthritis)
• Back Pain (osteomyeleitis and discospondylitis) • Abortion in pregnant women
• Headache
• Depression
• Insomia
Brucella
Regulatory Status
• SELECT AGENT
– USA PATRIOT Act and Public Health Security and Bioterrorism
Preparedness and Response Act of 2002
Reportable Infections in Texas
Brucella
• Brucella abortus in cattle
• Brucella melitensis in sheep and goats
• Brucella suis in swine
Francisella spp.
Characteristics
• Gram negative
• Non‐Motile
• Non‐spore forming • Siderophores
Francisella spp.
• Atmospheric – Obligate Aerobe
• Location – Facultative Intracellular
• Environment – Can persist in the environment: – for up to 6 months at 0°C
– up to 125 days in dust or soil – up to 1 year in feces
• Transmission – Direct contact, Ingestion, Inhalation
Francisella spp.
Virulence Factors
• Capsule
• Cellwall
• Acidphosphatase
– Suppresses respiratory burst of phagocytes
• TranscriptionalRegulators
– Igl—intracellular growth locus
• Prevents secretion of proinflammatory cytokines – Mgl—macrophage growth locus
• Prevents phagosome‐lysosome fusion • TypeIVSecretionSystem
Francisella spp.
Disease Syndrome in Dogs and Cats
• Infection
– Ingestion of infected animal (rabbit etc) – Tick bite
• Susceptibility is somewhat dependent on age – Younger animals are more susceptible
• Cats
– Older animals may be resistant
• Francisella tularensis
– F. tularensis subsp. tularensis (formerly biotype A)
– F. tularensis subsp. holartica
– F. tularensis subsp. novicida
– F. tularensis subsp. mediasiatica
Reservoir Hosts
• Francisella tularensis
• Lagomorphs – Rabbits
– Hares • Rats
• Mice
Vectors
• Francisella tularensis
Amblyomma americanum
Lone Star Tick
Lawnmower
Dermacentor variabilis
American Dog Tick
• Francisella tularensis
Diagnostics
• Incats
– Leukocytosis
– Thrombocytopenia
– Increased liver enzymes – Increased bilirubinemia
• ELISA
• Microscoicagglutination
• Fluorescentantibodytechniques
• Culture
– ONLY performed in laboratories with appropriate
biological containment
• Biosafety Level 3
• Francisella tularensis
Public Health Significance
• Human Symptoms of Tularemia:
– sudden fever
– chills
– headaches
– diarrhea
– muscle aches
– joint pain
– dry cough
– progressive weakness
CDC
– People can also develop pneumonia with chest pain, cough, and difficulty breathing.