exam 2 Flashcards

1
Q

camplobactor and helicobacter

A
  • Gram-negative ‘curvy’ organisms
  • Campylobacter – curved, comma or “seagull” shaped
  • Helicobacter – long spiral shaped “corkscrew” shaped
    -challenging to grow
    -BCL 2
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2
Q

natural host habitat of camplyobacter and helicobactor

A
  • Both genera are animal associated
  • Campylobacter
  • Intestinal tract (many species – birds and mammals)
  • Reproductive mucosa and gall bladder of cattle (C. fetus)
  • Helicobacter
  • Stomach and gastrointestinal tracts of mammals and birds
  • About 50% of us have H. pylori in our stomachs
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3
Q
  • Campylobacter jejuni virulence
A
  • Flagella – important for motility
  • Outer membrane adhesion proteins – adhesion
  • Superoxide dismutase and catalase – intracellular survival
  • Cytolethal-distending toxin – cell death
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4
Q

Campylobacter. fetus subsp venerealis bovine

A

-bovine causes vibrosis
-symptoms:* Silent carriage
* Temporary infertility
* Early embryonic death
* Abortions – rarely exceeds 10%
* Disease typically occurs when cows exposed for the first time
* Organism ascends from vagina to cause intrauterine infection
* Venereal transmission (natural or AI)
* Cows naturally clear infection
* Vaccination plays role
C. fetus subsp venerealis Vibriosis

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5
Q

Campylobacter. fetus subsp fetus sheep/ goats

A

Vibrosis
* Abortion in final 6 weeks of pregnancy in ewes
* May also see pyrexia and vaginal discharge
* Can also cause abortions in cattle
* Transmitted through ingestion
* Travels to gall bladder and pregnant uterus
* Highly contagious within a herd/flock
* Incubation period is 7-25 days
* Control abortion outbreaks with antimicrobials
* Vaccination plays role
-hepatic necrosis can be seen in fetus

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6
Q

C. fetus subsp fetus zoonosis

A
  • Reported human pathology includes
  • Septic abortions
  • Proctitis and proctocolitis
  • Sepsis
  • May be related to contact with animals
  • Possibly eating raw food
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7
Q

camplybacter. jejuni subsp jejuni humans

A
  • Common cause of gastroenteritis, self limiting 5-10 days.
  • Infection by ingestion
  • Unpasteurized dairy
  • Contaminated water
  • Poultry products
  • Very low infectious dose (<500 organisms)
  • 1 drop of raw chicken juice can make you sick
    -can lead to guillain Barre syndrome (rare)
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8
Q

Guillain-Barré
Syndrome

A

-C. jejuni subsp jejun
Rare sequelae (<1/1000 cases) following campylobacteriosis
* GBS is an acute demyelinating disease of the peripheral nerves
* Begins with weakness and tingling in extremities
* Can become systemic resulting in paralysis
* No known cure, but most people ultimately recover
* 20-40% of people with GBS were infected with Campy in the
last 3 weeks

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9
Q

Helicobacter spp.

A

-nobel prize for H. pylori being infectious agent of stomach ulcers.
-gastroenteritis in host animal. positive result can be in healthy animals.
-in dogs signs may be: vomiting, weight loss.
H pylori in cats, H. canis in dogs, cats and people.

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10
Q

Campylobacter and haemophilus resistance

A

-resistant to to trimetheprin, frisidic acid, streptogramins,

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11
Q

BRACHYSPIRA AND
LAWSONIA morph

A
  • BCL 2
    -gram neg swigly lines
  • Lawsonia intracellularis:
  • Obligate intracellular parasite
  • Can’t be grown outside of cell culture
  • Brachyspira spp.
  • Aerotolerant anaerobe
  • Do not typically form colonies
  • Challenging to grow
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12
Q

Brachyspira and Lawsonia host habitat

A
  • Lawsonia intracellularis
  • This is an obligate intracellular organism
  • Lives in the enterocytes of hosts
  • Brachyspira spp.
  • Found in the gastrointestinal tract of many species
  • Domestic and wild birds
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13
Q

Virulence Factors Brachyspira and Lawsonia

A
  • Lawsonia intracellularis: Type 3 secretion systems
  • Brachyspira spp:
  • Flagella – motility
  • Chemotaxis (attracted to mucous)
  • Hemolysins?
    -do not freeze samples
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14
Q

Lawsonia intracellularis pigs

A
  • Cause of proliferative enteritis (ileitis) - CORUGATION of mucosa is unifying lesion
  • Multiple forms of disease recognized
  • Intestinal adenomatosis: Hyperplasia of crypt epithelium
  • Necrotic enteritis: Chronic disease with mucosal necrosis
  • Regional ileitis: Chronis disease with thickening of muscularis layer of ileum
  • Proliferative hemorrhagic enteropathy: Can resemble swine dysentery
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15
Q

Lawsonia intracellularis horsees

A

-causes proliferative enteropathy
-young weaning foals 4-6 months
-weight loss, diarrhea, colotis
-fecal oral transmission
-can have granulatamous proliferative enteritis

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16
Q

Lawsonia intracellularis
hampters

A
  • Cause of “wet tail” in hamsters, clinical signs include
  • Diarrhea, dehydration
  • Anorexia
  • Death
  • Can have devastating outbreaks in large colonies
  • Most often affects weanlings (3-8 weeks)
  • Treat with antimicrobials and aggressive rehydration
  • Isolate affected animals
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17
Q

swine dysentery

A

-caused by brachyspira (B. hyodysenteriae &
B. hampsonii)
-in NA since late 2000
* Clinical signs include
* Diarrhea (#1) (mild and watery to muco-hemorrhagic)
* Inappetence
* Pyrexia
* Mortality in peracutely affected animals
* Most commonly seen in older pigs (grower finisher)
-incubation period 3-7days

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18
Q

B. hyodysenteriae
B. hampsonii

A

-causes swine dysentery
* Classically caused by B. hyodysenteriae
* Novel species have emerged over the last decade
* B. hampsonii – now very common in W. Canada
* Anecdotally the disease associated with B. hampsonii is less
severe than that associated with B. hyodysenteriae
* How to control the disease is a bit of a mystery
* Unclear exactly where it comes from (carriers, wildlife???)
* Antimicrobials in affected herds
* No effective vaccines available

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19
Q

brachyspira. pilosicoli pigs

A

-causes Spirochetal Colitis (less severe than swine dysentry)
* In finishing pigs: “Wet cement” feces without blood
* In younger animals may see more severe diarrhea (watery or mucoid
-usually self limiting
* Poor feed efficiency is a major concern with this disease.
-use antimicrobials, good manegement

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20
Q

Brachyspira spp. poultry

A
  • Domestic poultry species have been reported
    to be affected by a variety of Brachyspira spp.
  • B. alvinipulli
  • Associated with wet feces → diarrhea, green-yellow
    frothy cecal fluid
  • B. pilosicoli
  • Colonization of cecum associated with mucosal
    thickening
  • B. hyodysenteriae
  • Severe, necrotizing typhlitis in juvenile rheas (related to
    ostriches and emus)
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21
Q

Brachyspira spp humans

A
  • Intestinal spirochetosis
  • Brachyspira pilosicoli and aalborgi
  • In developing countries colonization with
    Brachyspira common (~30
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22
Q

Treponema spp. bovine

A

-causes digital dermatitis
* Likely a polymicrobial infection of the bovine foot
* Can present with proliferative (hairy heal warts) or
erosive lesions
* Suggests there may be a management problem
* Cattle standing in wet
* Topical (washing) for early lesions
* Topical antibiotics if more severe
* Oxytetracycline or lincomycin/spectinomycin

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23
Q

Brachyspira and Lawsonia treatment

A
  • Lawsonia:
  • Susceptibility testing impossible (obligate intracellular parasite)
  • Penicillins, bacitracin, aminoglycosides, virginiamycin and the ionophores DONT WORK
  • Therapy relies on macrolides/pleuromutilins
  • Brachyspira:
  • In pigs, treatment relies heavily on pleuromutilins and macrolides
  • Lack standardized methods
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24
Q

leptospira characteristics

A
  • Biocontainment level 2
  • Leptospira have 2 chromosomes
  • Culture is extremely challenging - slow growing (can take
    weeks)
  • Causes a constellation of disease syndromes in many species,
    these organisms inhabit multiple hosts and the epidemiology is
    complex
    -‘crooked ends’ when scanning with electron micrograph gram neg.
    -lab idenfity: in urine by dark field microscopy. or PCR. florecent antibody on liver and kidney.
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25
Q

leptospira host habitat

A
  • Maintained by animal hosts
  • Persist in renal tubules
  • Shed in urine
  • Contaminate environment
  • Water associated (rivers, ponds)
  • Readily survives in bodies of water
  • Moisture is very important for transmission
  • When possible, keeping animal housing dry and clean is an important control measure.
    -passed through water or direct contact with urine
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26
Q

leptospira virulence

A
  • Invade tissues through moist/softened skin, mucous
    membranes or by ingestion
  • Adhesions
    -surface surviving proteins
    -haeme oxygenase – allows utilization of haeme as iron source
  • Flagella – motility
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27
Q

Leptospira Hardjo
bovine

A
  • Infections most often without overt clinical signs
  • May result in reproductive problems
  • Reproductive failure
  • Abortion
  • Also associated with milk-drop syndrome
  • Mastitis
  • Flabby udder
  • Yellow or red tinged milk
  • Chronic genital infection common
  • Shed in urine possibly for life
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28
Q

Leptospira Pomona bovine

A
  • Acute infections much more apparent
  • Fever, anorexia, lethargy, decreased milk production
  • Haemolytic anemia, intravascular hemolysis, petechiation. isrertic fetal tissues.
    -treatment depends on type of symptoms: antimicrobials and supportive care
    -prevention: vaccines, dry environment, eliminate carriers
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29
Q

Leptospira Pomona swine

A
  • Persists in the kidney and are shed in the urine
  • Clinical disease typically seen in gilts
  • Acute: Pyrexia, listlessness
  • Chronic: Abortions, Considerable economic loss
    -milk spot kidney
  • Infections with Leptospira Icterohaemorrhagiae, Canicola,
    Australis, Grippotyphosa and Hardjo reported
  • Be aware of maintenance host and control as appropriate
30
Q

Leptospira swine treatment

A
  • Treatment
  • Antimicrobials important when dealing with outbreaks
  • Apparently not effective at eliminating serovars from herds which are
    maintained by pigs
  • Control measures
  • Replacement stock are the most likely source for a herd
  • Biosecurity, skunks have been implicated in outbreaks
  • Vaccination
  • Interruption of transmission is most important
31
Q

leptospira dogs

A

-Younger animals are more severely affected
* Clinical signs include:
* Pyrexia
* Vomiting, dehydration, diarrhea (melena)
* Peripheral vascular collapse, tachypnea, poor capillary perfusion
* Icterus (liver is also damaged)
* Peracute infections can result in massive leptospiremia and rapid death
* See most commonly in hounds and working dogs
* Probably those animals with more wildlife or contaminated water body contact
Leptospira
-hot spots are southern ontario and nova scotia

32
Q

leptospira dogs treatment

A
  • Antimicrobials
  • Penicillin is the treatment of choice for acute disease
  • Tetracyclines, macrolides or aminoglycosides needed to eliminate carrier state
  • Prevention
  • Vaccines are available
  • May prevent disease but not carrier state (zoonotic risk!)
  • Avoid contact with reservoirs
    Leptospira
33
Q

leptospira humans

A
  • Acute onset fever, headache, muscle pain and conjunctivitis
  • Can mimic dengue
  • Can also have icterus (5-10% of cases)
  • Case fatality rate typically (1-5%) without treatment, up to 20%
    if hepatorenal failure without dialysis
  • Occupational exposure very important
  • Workers on farms, mines, sewers, abattoirs, vet, fish, dairy and milkers.
    -incubation 10 days, rare in NA. travel infection.
34
Q

Zoonotic/Interspecies Transmission of leptospira

A
  • Animal → Animal and Animal → Human very important
  • Very broad host range including wild and domestic mammals,
    reptiles and amphibians
  • A 1983 study found that 90% of rats in Detroit were positive for
    Leptospira Icterohaemorrhagiae
  • In Europe beware the hedgehog
  • Personal protective equipment should be utilized
    to avoid direct contact with infected animals
35
Q

leptospira treatment don’t use

A
  • A wide variety of drugs can be used, beware of
    what species you are treating and what the drug
    withdrawal times may be
  • What is your goal? Clinical cure or clearing
    carriers?
  • Streptomycin, doxycycline
  • Chloramphenicol and the sulfonamides are NOT
    recommended
36
Q

Taylorella and Bordetella characteristics

A

-small gram neg cocco bacilli
-BCL 2
- Taylorella equigenitalis is a notifiable disease in Canada
* Taylorella
* Carboxyphilic, facultative anaerobe
* Bordetella
* Obligate aerobes
* Non-fermentative
* Highly contagious!

37
Q

Taylorella and Bordetella host habitat

A
  • Taylorella
  • Host associated
  • In the equine genital tract
  • Bordetella
  • Respiratory tract of many species
  • Healthy and diseased animals
    -do not survive well in environment
38
Q

bordatella virulence

A
  • Adenylate cyclase haemolysin – inhibits phagocytosis, and local
    immune response
  • Dermonecrotic toxin - broadly important among Bordetella
  • Amount of toxin produced may be related to strain virulence
  • Inhibitory towards porcine osteoblasts (atrophic rhinitis)
  • Also required for B. avium to be pathogen
39
Q

B. pertussis, Pertussis Toxin

A
  • Pertussis toxin
  • The activity of this toxin is believed to be responsible for
    whooping cough
  • Composed of 5, 2-part subunits (A/B)
  • A subunit ultimately leads to increased cAMP levels
  • Affecting cell signaling
  • Also has systemic effects
  • ↑ insulin
  • Inhibits recruitment of WBC and affects chemokine production
40
Q

taylorella equigenitalis

A

*causes Contagious equine metritis
* In mares:
* Vaginal discharge 2-7 days after breeding
* Return to estrous
* In stallions:
* Doesn’t typically result in clinical disease, silent carriers
* Found in smegma accumulating in the urethral fossa
* Venereal disease in horses
* Natural mating or AI

-CFIA reportable
-treatment: antimicrobials, washing of vulva and clitoris and clitoral fossa.
-control: stud selections, import
-test horse from endemic region and quarentine.

41
Q

bordetella avium.

A

-causes turkey coryza
* Disease of upper respiratory tract
* Sneezing (called snick)
* Nasal discharge (mucoid, tenacious exudate)
* Altered vocalization
* Mouth breathing
* Highly infectious - up to 100% of flock affected
* Affects young birds (<4 weeks
-low mortaltity but could be high with secondary invadors

  • Transmission:
  • Direct contact
  • Contaminated feed, water, litter
  • Survives in environment for 1-6 months!
  • Also occurs in chickens although
    disease tends to be less severe
  • Treatment
  • Antimicrobials (tetracyclines)
  • Control
  • Vaccinations
  • Biosecurity
42
Q

bordetella bronchispetica pigs

A
  • Associated with infections of the respiratory tract in young pigs
  • Pneumonia
  • Atrophic rhinitis
  • Atrophic rhinitis caused by complex of P. multocida (PM) type D
    or A and B. bronchiseptica (BB)
43
Q

what causes atrophic rhinitis / path

A
  • Atrophic rhinitis caused by complex of P. multocida (PM) type D
    or A and B. bronchiseptica (BB)
  • BB starts the infection, causes damage allowing PM to proliferate
  • Toxins produced by PM cause epithelial hypoplasia, atrophy of mucous
    glands, osteolysis
  • Dermonecrotic inhibits osteoblasts
  • Ultimately results in atrophy of nasal turbinates and shrinking of snout
44
Q

bordatella bronchiseptica dogs

A
  • Cause of kennel cough (canine infectious tracheobronchitis)
  • Often polymicrobial infection
  • Acute onset clinical signs
  • Paroxysmal, productive cough with retching
  • Swollen vocal cords result in unusual sounding cough (honk)
  • Disease usually self-limiting
  • Incubation period 3-10 days
  • Very contagious

Patient history is an important part of the diagnosis
* Lack of vaccine in past 6 months
* Contact with other dogs
* Treatment
* Antimicrobials in severe cases
* Supportive therapy
vaccines: oral, intranasal, sub Q

45
Q

bordatella bronchiseptica cats

A
  • Disease less common than in dogs
  • May be associated with contact with infected dogs
  • Clinical signs include
  • Sneezing
  • Mucopurulent nasal and ocular discharge
  • Often mild compared to dogs
  • Cough is UNCOMMON!
  • Disease more severe (pneumonia) in young kittens
  • Treatment
  • Doxycycline
46
Q

B. bronchiseptica rabbits

A
  • Like pigs, we see similar diseases in rabbits caused by B.
    bronchiseptica and P. multocida
  • Rhinitis
  • Pneumonia
  • Otitis media/interna
  • Very common in rabbits with respiratory disease up to 50%
    -causes sniffles
47
Q

B. bronchiseptica Guinea
Pigs

A
  • Guinea pigs are among the most susceptible species to
    Bordetella infections
  • Infection more likely to lead to serious disease than carrier state
  • Acute, rapidly progressive respiratory infections with high
    mortality rate
  • Rabbits can also serve as reservoir for more susceptible
    species such as guinea pigs
48
Q

B. pertussis people

A

-causes whooping cough
* Disease progresses through 3 phases
* Prodromal phase:
* Cold or flu like illness
* Paroxysmal phase:
* Begins 7-14 days after prodromal phase
* Coughing paroxysms, followed by desperate gasps for air
* Paroxysms often followed by cyanosis and vomiting
* Convalescent phase:
* Within 4 weeks on onset
* Decreased occurrence of paroxysms

Atypical pertussis occurs in adults
* Relatively common in university students, military personnel
-350000 deaths anually
-vaccines
-highly contagios

49
Q

sample Collection and Handling of bordetella

A

Bordetella spp.
* Nasal or tracheal swabs
* Do NOT use cotton swabs, cotton can be toxic to these organisms and
reduce the likelihood of recovery
* Bronchoalveolar lavage
* Transtracheal wash
* Transport media is important
* Do NOT freeze
-culture, serology, florencent antibody test

50
Q

Zoonotic/Interspecies Transmission
* Taylorella and bordetella

A
  • Taylorella only causes clinical diseases in equids
  • Bordetella species should all be considered potentially zoonotic
  • We have insufficient evidence to quantify risk
  • B. bronchiseptica has been isolated from respiratory
    submissions from people including whooping cough like illness
  • Can be pathogenic in compromised patients
  • Children
  • Chronic alcoholics
  • AIDS
  • Acute leukemia
51
Q

dimorphic fungi characteristics

A
  • These organisms assume 2 forms( Mycelial (mold) and yeast forms)
    -thermally dimorphic fungi depend on temp for growth. yeast as body temp and above 37.
  • Biocontainment level 3 – when in mycelial form
  • Biocontainment level 2 – when in yeast form
    -budding yeast looking at 37 or stringy in mycelial phase
52
Q

dimorphic fungi environment

A
  • These are all environmental organisms
  • Blastomyces dermatitidis – acidic soils (water, creek)
    -* Coccioioides immitis – soil of low elevation deserts
  • Histoplasma capsulatum – nitrogenous soils (bat/bird feces)
  • Sporithrix schenckii complex – old wood
    -all common with resp infections.
    -urine antigen samples, aspirates, excudates from lesions.
    -use serology or cytology
    -DANGEROUS when cultured.
53
Q

dimorphic fungi morph

A

-blasomyces dermatitdis: myceal phase long rods look like sperm
-Mycelial phase of Coccidioides
immitis. has a barrel shaped arthroconidia
-Histoplasma capsulatum mycelial phase. Note the large tuberculate macroconidia and the
small microconidia.
-Sporothrix schenckii. mycelial phase, clusters of conidia with a floral distribution

54
Q

geographical dimorphic fungi

A

-blastomyces (southwest can, ON) or africa
-coccidioides (SE USA)
-histoplasma (SW Cad, south USA)
-sporothrix (USA, mexico, china, brazil)

55
Q

dimorphic fungi pathogenesis

A

-blastomyces: spores in enviro in mycelial phase then inhaled or into skin.
-coccidiosis: inhaled, tiny move in wind, go to alveioli. make endospores with spherules.
-histoplasma: spores in mycelial phase then inhaled to LN and throughout body.
-sporothrix: in enviro with traumatic plant material (rose bushes, hay, ect)

56
Q

Blasytomyces. dermatidis dogs

A

-most common in sask
-respiratory disease, use rads of lungs with nodular lesions
-ocular signs (uveitis)
-skin lesions 20-50% time
-chronic sick: anorexia, weightloss, lameness
-previous antibiotic therapy
-common in young dogs, sporting breeds.
-by water or dirt excavation dogs 10x more s than people.

57
Q

Blasytomyces. dermatidis people

A
  • Most often starts as respiratory infection
  • Dry cough
  • Fever
  • Weight loss
  • Bone is most common site of extra-pulmonary involvement
  • The state of Mississippi is the most highly endemic region
  • If you suspect that your patient has Blastomyces, ask the owners about clinical disease in their family members!
58
Q

coccidodies clinical dogs/cats

A
  • Disease colloquially known as “Valley Fever
  • Subclinical infections common
  • Up to 70% of dogs
  • Clinical signs depend on site of infection:
  • Lameness most common
  • Chronic illness
  • Respiratory signs, granulomatous pneumonia.
  • Lymphadenopathy
  • Non-healing cutaneous lesions (cats usually)
    -see after rainfall then dust in AZ
    -latenent infection up to 3 years.
  • Treatment
  • Amphotericin B, fluconazole, itraconazole
59
Q

Histoplasma capsulatum
dogs

A
  • Most infected animals have disseminated disease, wide range of non-specific signs
  • Depression, weight loss, fever most common clinical signs, draining tracts
  • Unresponsive to antibiotics
    Diarrhea – due to Histoplasma enteritis
  • Often large bowel diarrhea with mucous and frank blood
  • Hepatomegaly
  • Splenomegaly
  • Icterus
    -may be self limiting or use antifungal: * Amphotericin B
60
Q

Histoplasma capsulatum cats

A
  • Cats are very susceptible
  • 2 nd most commonly reported systemic mycosis in cats
  • Most have disseminated disease with non-specific signs
  • Skin lesions (nodules or ulcers) common
  • Respiratory signs OTHER than cough
  • Dyspnea, tachypnea and abnormal lung sounds
  • Ocular involvement in ~1/4 of cats
61
Q

S. schenckii complex
horses (most common)

A
  • Most often presents as a lymphocutaneous disease
  • Nodules develop at the site of infection
  • Eventually nodules and cutaneous lymphatics ulcerate
  • Exudation of yellowish exudate from ulcers
  • Disseminated disease can develop if cutaneous or
    lymphocutaneous forms not treated
    -ulcerative dermatitis
  • Disease develops after damage to skin from contaminated plant
    material
  • Thorns for example
  • Treatment: Systemic iodine
    preparations=Itraconazole
62
Q

S. schenckii complex cats

A

-feline sporotrichosis causes cutaneous and extracutaneous forms.
-single or multiple skin lesions, usually with nose mucosa. nodules and skin ulcers.
-extracutaneous: resp signs, swollen LN, cartilage and bone lesions.
-lesions on face and nose of cats.

63
Q

S. schenckii complex people

A
  • Associated with
  • Sphagnum moss, rose bushes and splinters
  • S. brasiliensis
  • Zoonotically acquired from cats (bites/scratches)
  • As of fall 2023, geographically limited to South America
  • Get small painless pustules, then get multiple linearly placed secondary pustular lesions or ulcerating lesions along proximal lymphatics
    -zoonotic from bites/ scratches.
64
Q

histophilus and glasserella characteristics

A

-gram neg cocco-bacilli
-BCL 2
-* Facultative anaerobes
* Fastidious
-part of normal microbiota
* Histophilus somni: Respiratory and reproductive tract
* Glaesserella parasuis: pigs, resp, membranes, genital tract
-factors X and V

65
Q

glasserela parasuis virulence

A
  • Capsule – adhesion and invasion
  • Fimbriae – associated with encapsulated strains
  • Lipooligosaccharide – toxic lipid A component, also capable of phase
    variation → antigenic variation and immune evasion
  • Glaesserela parasuis induces cells to eat it (autophagy) as a strategy
    for getting into cells!
66
Q

Histophilus somni bovine

A
  • Often involves more
    than one organ system
  • Respiratory infection
    (shipping fever)
  • Fever, tachypnea, cough,
    nasal discharge
  • Can be fatal
  • Pain associated with pleuritis
  • Thrombotic
    meningoencephalitis
  • Septicemia
  • Myocarditis – sudden death
  • Arthritis
  • Abortion
  • Enzootic calf pneumonia.
    -vascular thrombosis
  • Tissue infarction + necrosis with haemorrhage. vascular thrombosis
  • Thrombotic meningoencephalitis in older calves and yearlings
  • Depression, fever, blindness, coma and sudden death
  • Treatment
  • Antimicrobials
  • Control
  • Vaccination
67
Q

histophilus somni sheep

A

-* Lameness, septicemia, epididymitis-orchitis, metritis, abortion and
mastitis
-necrositing myocarditis, firbrous broncho. ect.

68
Q

glasserella parasuis

A
  • Presentation depends on site of infection
  • In naive herds see rapid onset of disease
  • Pyrexia, inappetence, anorexia
  • Abortion in gilts
  • Lameness chronically
    -septicemia- sudden death.
    -glassers disease: fibrinous polyserositis.
    -disease in mixing herds, young pigs 4-8 weeks. short 1-5d incubation.
69
Q

glasserella parasuis treatment and control

A
  • Treatment
  • High doses of antimicrobials early in course of disease
  • Control
  • Vaccination of gilts (ensuring protective maternal immunity)
  • Beware of new introductions
  • Not mixing litters
  • Adequate colostrum intake
70
Q

Haemophilus influenzae people

A
  • Found in the oro/naso pharynx of up to 85% of people
  • Clinical signs depend on site of infection
  • Fever and chills, cough, difficulty breathing
  • Associated with wide variety of diseases
  • Meningitis, otitis media, epiglottitis.
  • Before vaccines this was the most common cause of bacterial
    meningitis in kids 1 month – 2 years.
    -hearing loss.
71
Q

Haemophilus influenzae people treat and common

A
  • Vaccines J
  • Unvaccinated children
    are most at risk
  • Beware of schools,
    daycares
    Common themes
    1.Colonizes upper respiratory tract
    2.Multisystemic disease
    3.Occurs when susceptible populations mix
72
Q

histophilus and glasserella treatment and samples/ resistance

A

-joint fluid, tissues with lesions.
-do not freeze, get to lab quickly
-host specific strains not zoonotic
* Treatment
* Antimicrobials early in infection helpful
* Macrolide type drugs can be useful
* Erythromycin
* Vaccines important (Glaesserella parasuis)
* Intrinsic resistance to streptogramins (virginiamycin)