exam 2 Flashcards

(72 cards)

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
leptospira host habitat
* 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
26
leptospira virulence
* 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
27
Leptospira Hardjo bovine
* 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
28
Leptospira Pomona bovine
* 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
29
Leptospira Pomona swine
* 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
Leptospira swine treatment
* 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
leptospira dogs
-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
leptospira dogs treatment
* 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
leptospira humans
* 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
Zoonotic/Interspecies Transmission of leptospira
* 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
leptospira treatment don’t use
* 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
Taylorella and Bordetella characteristics
-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
Taylorella and Bordetella host habitat
* 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
bordatella virulence
* 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
B. pertussis, Pertussis Toxin
* 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
taylorella equigenitalis
*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
bordetella avium.
-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
bordetella bronchispetica pigs
* 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
what causes atrophic rhinitis / path
* 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
bordatella bronchiseptica dogs
* 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
bordatella bronchiseptica cats
* 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
B. bronchiseptica rabbits
* 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
B. bronchiseptica Guinea Pigs
* 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
B. pertussis people
-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
sample Collection and Handling of bordetella
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
Zoonotic/Interspecies Transmission * Taylorella and bordetella
* 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
dimorphic fungi characteristics
* 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
dimorphic fungi environment
* 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
dimorphic fungi morph
-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
geographical dimorphic fungi
-blastomyces (southwest can, ON) or africa -coccidioides (SE USA) -histoplasma (SW Cad, south USA) -sporothrix (USA, mexico, china, brazil)
55
dimorphic fungi pathogenesis
-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
Blasytomyces. dermatidis dogs
-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
Blasytomyces. dermatidis people
* 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
coccidodies clinical dogs/cats
* 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
Histoplasma capsulatum dogs
* 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
Histoplasma capsulatum cats
* 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
S. schenckii complex horses (most common)
* 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
S. schenckii complex cats
-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
S. schenckii complex people
* 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
histophilus and glasserella characteristics
-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
glasserela parasuis virulence
* 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
Histophilus somni bovine
* 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
histophilus somni sheep
-* Lameness, septicemia, epididymitis-orchitis, metritis, abortion and mastitis -necrositing myocarditis, firbrous broncho. ect.
68
glasserella parasuis
* 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
glasserella parasuis treatment and control
* 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
Haemophilus influenzae people
* 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
Haemophilus influenzae people treat and common
* 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
histophilus and glasserella treatment and samples/ resistance
-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)