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NSB II > Bacterial Pathogens of the Nervous System > Flashcards

Bacterial Pathogens of the Nervous System Flashcards

1
Q

describe otitis media and otitis interna

A

media:
1. inflam of middle ear
2. often extension of infection in external ear or penetration of tympanic membrane by foreign object; RARELY hematogenous spread

interna:
1. inflam of inner ear
2. extension from infection in middle ear; RARELY hematogenous spread

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2
Q

describe discospondylitis

A
  1. inflam of vertebral disc and adjacent vertebral bodies
  2. caused by hematogenous spread of organisms (often from skin or urinary tract) to vertebral endoplate and spreads to disc
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3
Q

describe ulcerative keratitis (corneal ulcer)

A
  1. often results from injury to eye
  2. infection results from bacteria on animal or in animal’s environment
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4
Q

what are 5 common bacterial causes of otitis media and interna, discospondylitis, and ulcerative keratitis?

A
  1. streptococcus canis
  2. staphylococcus pseuintermedius
  3. escherichia coli
  4. pseudomonas aeruginosa
  5. brucela canis: can cause discospondylitis
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5
Q

describe streptococcus spp.

A
  1. gran positive cocci, facultative anaerobes
  2. many (not all) species are normal microbiota that live on mucus membrane of upper resp, GI, or lower gnital tracts
  3. infections associated with strong neutrophilic (pus/abscess) response
  4. S. canis is primary found in dogs and cats
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6
Q

describe streptococcus spp. pathogenic features and virulence

A
  1. M protein: fibular surface protein: MOS IMPORTANT virulence determinant; allows adherence to epithelial cells
  2. polysaccharide capsule: interferes with phagocytosis and complement-mediated lysis
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7
Q

describe transmission of streptococcus spp.

A
  1. endogenous infections common
  2. exogenous via direct contact with infected animals, aerosol inhale, and fomite transmission (survive in dried pus for weeks)
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8
Q

describe streptococcus spp. clinical disease

A
  1. opportunistic! normal microbiota of skin, ears, mucous membranes in dogs and cats
  2. common cause of ear infection (most commonly externa)
  3. occasional cause of pneumonia secondary to resp viral disease
  4. diagnosis: lab culture/ID with antibiotic suscpetibility
  5. treatment: antibiotics
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9
Q

describe staphylococcus spp.

A
  1. gram positive cocci, often found in clusters; live on skin and mucosal surfaces
  2. invades upon epithelial damage = OPPORTUNISTS
  3. disease characterized by strong pus (neutrophilic inflam) response
  4. S. pseudintermedius primary spp in dogs and cats
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10
Q

describe transmission of staphylococcus spp.

A
  1. endogenous most common
  2. exogenous infections can occur by direct contact with infected host or bi indirect fomite spread
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11
Q

describe clinical disease of staphylococcus pseudintermedius

A
  1. normal microbiota of dog and cat skin, ears, throat, nasal, and genital mucosa = opportunistic
  2. common cause of ear infection (most commonly externa)
  3. common cause of pyodermia (skin infection) in dogs and cats follow skin trauma (scratching due to dry skin, allergies, fleas/mites)
  4. common cause of cystitis with struvte calculi
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12
Q

describe diagnosis and treatment of staphylococcus pseudintermedius spp.

A

diagnosis: lab culture/ID with anitbiotic susceptibility

treatment: appropriate antibiotics
-often secrete beta lactamase!

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13
Q

describe pseduomonas aeruginosa spp.

A
  1. gram negative rod
  2. an environmental organism, but some healthy animals carry on skin, mucus membranes (but transiently, not normal microbiota)
  3. produces characteristic blue green pigments
  4. characteristic odor: grape or tortilla chips
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14
Q

describe pseduomonas aeruginosa spp. pathogenic features and virulence

A

tendency to form biofilms (alginate polysaccharide)

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15
Q

describe pseduomonas aeruginosa spp. transmission

A
  1. endogenous (transient organism) or exogenous from environment- OPPORTUNISTIC INFECTION
  2. exploits compromise in host defenses:
    -breaks in skin
    -prolonged wetting of skin or ears
    -burns
    -IV or urinary catheters
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16
Q

describe pseduomonas aeruginosa spp. clinical disease

A

dogs and cats: otitis externa, conjunctivitis/ulcerative keratitis, UTI

horses: metritis, conjunctivitis/ulcerative keratitis

cows: mastitis, metritis, skin infections, UTI

sheep and goats: mastitis, pneumonia

pigs: otits externa, enteritis, pneumonia

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17
Q

describe diagnosis and treatment of conjunctivits/ulcerative keratitis

A

dx: lab culture/ID with antibiotic susceptibility testing (important bc intrinsically resistant to many commonly used Ab)
-has Ab efflux pumps, secretes beta lactamase, and forms biofilms

tx: appropriate Ab

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18
Q

describe escherichia coli

A
  1. gram negative rod; normal microbiota of animal intestines
  2. MOST e. coli strains are opportunists; disease caused by fecal contamination of sites but SOME strains ARE primary pathogens
  3. primary pathogen strains broadly divided into either intestinal or extraintestinal pathogenic strains
    -intestinal: commonly cause diarrhea, often in neonatal calves, lambs, piglets, foals
    -extraintestinal: invasive and wide variety
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19
Q

describe pathogenic features and virulence of escherichia coli

A
  1. polysaccharide capsule: interferes with phagocytosis
  2. various fimbriae/pili: adherence
  3. lipopolysaccharide (LPS or endotoxin): released upon bacterial death; causes fever, endothelial cell damage, shock
  4. various toxins:
    -enterotoxins: cause fluid secretion into intestinal lumen (diarrhea)
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20
Q

describe transmission of escherichia coli

A
  1. endogenous from own microbiota
  2. exogenous from environment, feed, water, or fomites within feces
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21
Q

describe clinical disease of escherichia coli

A

affects many hosts and causes many types of diseases

  1. diarrhea: babies esp
  2. UTIs
  3. otitis
  4. speticemia
  5. mastitis
  6. meningitis
  7. respiratory infection
  8. eye infection
  9. surgical site infection
22
Q

describe diagnosis/treatment/prevention of escherichia coli

A

diagnosis: lab culture/ID with Ab susceptibility

treatment: appropriate Ab; fluids and electrolytes and supportive care for diarrhea

prevention: keep feed, water, and housing environment clean (remove feces)

23
Q

describe brucella spp.

A
  1. gram negative coccobacilli
  2. pathogen of repro organs
    -causes abortion in cattle, swine, sheep, goats
    -B. canis found in dogs
  3. does NOT replicate outside of host but CAN persist in environment in contaminated abortive tissues, genital tract secretions
  4. mandatory brucellosis control program to keep B, abortus out of dairy herds
  5. ZOONOTIC agent; consumption in nonpasteurized products or contact with infected animal
  6. confirmed infection in ANY species is REPORTABLE
24
Q

describe brucellosis spp. pathogenic features and virulence

A
  1. facultative intracellular pathogen of macrophages
  2. inhibition of phagosome fusion with lysosome fusion; replicates intracellularly in phagosome
  3. endotoxin (LPS): certain LPS mutations result in attenuation and are basis for bovine vaccine strain
25
Q

describe transmission and pathogenesis of brucellosis spp.

A
  1. by contact of mucous membranes with organisms in vaginal secretions, semen, aborted fetus, placenta, urine, blood, milk, and other organs of infected animals
  2. also inhalation of aerosols or ingestion
  3. bacteria penetrates mucous membranes; phagocytosed by macrophages and carried to regional lymph nodes
  4. bacteremia develops and bacteria spread to other nodes, to many organs, but prefer the uterus, udder, epididymis, testes for replication
26
Q

describe clinical disease of brucellosis spp.

A

also called brucellosis

  1. abortion
  2. epidiymitis
  3. orchitis
  4. placentitis
  5. mastitis
  6. arthritis
  7. discospondylitis: B. canis causes 10% of these cases in dogs
27
Q

describe diagnosis and treatment of canine brucellosis

A
  1. look for antibody to B. canis in serum
  2. mercaptoethanol rapid slide agglutination test (ME-RSAT)/card test: inexpensive, quick, uses dyed killed whole B.canis cells mixed with serum and looking for agglutination
  3. if any test positive is reportable!!! inform owner of health risk in keeping infected dog
  4. treatment:
    -longterm (90d) Ab therapy
    -neuter dog to reduce shedding
28
Q

describe listeria monocytogenes

A
  1. gram positive rod
  2. ubiquitous in nature; commonly found in soil, water, farm animal feed, and LARGE NUMBERS in spoiled silage
  3. some clinically normal people and animals can be fecal shedders
29
Q

describe listeria monocytogenes pathogenic features and virulence

A
  1. facultative intracellular bacterium of many host cells; including epithelial cells, liver cells, macrophages, neural cells, and trophoblast cells of placents
  2. lyses phagosome membrane allowing escape from phagosome into host cell cytosol; spreads to adjacent cells without entering extracellular environment
30
Q

describe listeria monocytogenes transmission

A
  1. primary route is ingestion!
  2. large numbers found in spoiled silage (pH >5.5) and bacteria multiply; disease more common in winter
  3. exposure via ingestion is common but disease is rare!
    -disease more common in immunocompromised host
  4. transit via oropharynx along nerves (trigeminal branches) to CNS (brainstem)
  5. may also exit along nerves from eye or nose to CNS
  6. ingestion may lead to infection of trophoblast cells and abortion
31
Q

describe listeriosis neural form

A
  1. circling disease: meningoencephalitis
  2. symptoms:
    -fever
    -multiple unilateral cranial nerve deficits with altered mentaion
    -propulsive walking
    -tendency to circle to one side
    -head tilt
    -nystagmus
    -head pressing
  3. histopathology: microabscesses in affected CNS areas
32
Q

describe diagnosis and treatment of listeriosis

A

diagnosis:
1. history and clinical signs
2. necropsy with histopath showing multifocal microabscesses in the brainstem
3. demonstration of organism by immunohistochemistry with antibodies specific for listeria

treatment: Ab

33
Q

describe clostridum spp.

A
  1. gram positive ANAEROBIC rods
  2. disease are toxin based, produce spores to persist in environment
  3. C. tetani and C. botulinum produce neurotoxins
34
Q

describe clostridium tetani

A
  1. organism/spores present in soil
  2. infection from contamination of wounds or umbilical stump
  3. spores germinate in devitalized traumatized (necrotic) tissue, vegetative (actively growing) bacteria release toxin
  4. disease is due to tetanospasmin toxin which enters bloodstream/lymphatics and is absorbed by motor nerves
35
Q

describe pathogenesis and clinical disease of tetanus

A
  1. toxin passes up peripheral nerve axon to spinal cord and brain
  2. toxin irreversibly binds to inhibitory neurons in CNS
  3. blocks release of inhibitory GAGA from inhibitory interneurons in spinal cord and results in excitation of motor neurons
  4. clinical disease: spastic paralysis (tonic contractions) of muscles
36
Q

describe diagnosis of tetanus

A
  1. generally based on clinical signs +/- history of wound (may have healed over by time see disease)
  2. culture difficult and unrewarding
37
Q

describe treatment/prevention of tetanus

A
  1. supportive care
  2. debride and clean wound if present
  3. administer antitoxin to neutralize any unbound circulating toxin (may be of little value)
    -recovery depends on development of new axon terminals (takes weeks)

prevention: active immunization with toxoid

38
Q

describe clostridium botulinum

A
  1. spores common in intestine
    -when animals die, spores germinate under moist anaerobic conditions and vegetative bacteria emerge and generate the neurotoxin which contaminates the carcass and surrounding plant material
  2. transmission: usually toxin ingestion!
    -wound contamination with spores also possible
    -toxin absorbed from intestinal tract, enters bloodstream, transported to peripheral nerves
  3. flaccid motor paralysis results; more toxin leads to more rapid progression of signs; potentially fatal
39
Q

describe pathogenesis of botulism toxin

A
  1. neurotoxin taken up by presynaptic protion of peripheral cholinergic synapses (NMJ) of motor nerves to prevent Ach release; synapse degenerates (once Ach release is blocked, muscle cannot contract)
  2. can occur by respiratory failure
  3. MOST POTENT neurotoxin known
40
Q

describe botulism signs in horses/ruminants

A
  1. slow to consume feed, dysphagia, decreased tongue tone
  2. muscle weakness, exercse intolerance, shuffling, staggering gait, recumbency
  3. mydriasis (dilated pupil); in advanced cases see eyeled paralysis
  4. decreased borborygmus (gut motility)
  5. bladder distension
  6. rare in dogs and cats but same signs if develops
41
Q

describe diagnosis of botulism

A
  1. usually by exclusion; routine lab work is normal

2 definitive: toxin ID by ELISA on feed, in serum, tissues, stomach, rumen, or intestinal contents, feces

42
Q

describe treatment of botulism

A
  1. antitoxin to ruminants and horses if available
    -ties up circulating toxin but NO effect on bound toxin; recovery is both growth of new presynaptic nerve endings
  2. supportive nursing care is essential
  3. Ab generally only for secondary infections
  4. rest! muscular activity consumes Ach and worsens signs
43
Q

describe mycoplasma spp.

A
  1. gram negative variable shape
  2. very small genome; limited biosynthetic capabilities, must coexist with a host; OBLIGATE extracellular bacterium
  3. NO CELL WALL; so are pleomorphic and don’t survive well outside host
  4. usually host species specific!
  5. many species are normal flora or mucous membranes and are never associated with disease
  6. divided into hemotrophic (infect RBCs) and non-hemotrophic types (infect epithelial cells)
44
Q

describe M. felis

A
  1. non hemotrophic mycoplasma
  2. endogenous transmission: commensal of conjunctiva and upper respiratory tract of cats
  3. clinical disease:
    -occurs when overgrowth of organism
    -can cause conjunctivitis
  4. diagnosis: PCR of conjunctival swab
  5. treatment: Ab
45
Q

describe chlamydiae

A
  1. gram negative rods or cocci
  2. obligate intracellular; have a cell wall but canNOT replicate without host
  3. chlamydia and chlamydophila are important
  4. infect epithelial cells of conjunctiva, resp, GI, genitourinary mucosa cells of CARRIER animals
  5. carrier: nonusual presence in a host of potentially pathogenic bacteria that may not be harmful to carrier but is potentially dangerous for others exposed to the carrier
46
Q

describe chlamydiae pathogenic features and transmission

A

two phase developmental cycle

  1. infectious form is extracellular elementary body (EB, metabolically inactive) take up by cells and converts to replicative and metabolically active reticulate body (RB) which are in phagosome which doesn’t fuse with lysosomes
  2. RB transforms back to EB after 2-3 days and are released by cell lysis

transmission: EBs spread by direct contact, aerosol, or ingestion

47
Q

describe clinical disease of chlamydia felis; also give diagnosis, treatment, prevention

A
  1. resemble non-hemotrophic mycoplasma infections
  2. conjunctivitis in young cats (<1year)
  3. primary mode of transmission via transfer from genital mucosa of carrier queen during parturition
  4. clinical disease often stress induced

diagnosis: PCR from conjunctival swab

treatment: Ab

prevention: vaccine for at risk populations (shelter)

48
Q

describe rickettsia rickettsii

A
  1. gram negative coccobacilli
  2. obligate intracellular
  3. causes rocky mountain spotted fever: a seasonal tick borne disease that affects dogs and humans throughout USA
  4. reservoir and vector ticks: Dermacentor andersoni, D. variabilis, Rhipicephalus sanguineus
49
Q

describe rickettsia rickettsii transmission

A
  1. infected eggs laid
  2. larvae feed on small mammals (rodent chipmunk, squirrel)
  3. develop into infected nymphs and then adult which feeds on dog or human
50
Q

describe pathogenic features and pathogenesis of describe rickettsia rickettsii

A
  1. enter circulation, invade and replicate in endothelial cells of small arteries and veins
  2. possess phospholipase, which damages endothelial cell membranes, resulting in inflammation and vasculitis develops due to increased permeability
51
Q

describe clinical signs, diagnosis, treatment, and prevention of describe rickettsia rickettsii (RMSF)

A

clinical signs:
1. rash, edema
2. small hemorrhages (petechiae) on mucous membranes
3. joint and muscle pain
4. renal disease
5. encephalitis and spinal cord disease

diagnosis:
1. clinical signs
2. seasonal occurrence
3. serological tests looking for antibody increase

treatment: Ab

prevention: tick control only there is no vaccine

NSB II (17 decks)

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