Lecture 15: Infections of the Urogenital System III

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32 Terms

1
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What pathogen causes enzootic abortion of ewes (EAE)?

chlamydia abortus

2
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What is the general morphology of chlamydia abortus?

  • spherical intracellular bacteria with unique developmental cycle

  • Energy parasites (unable to synthesize ATP)

  • cell walls lack peptidoglycan, but contain family-specific LPS

3
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Describe the virulence and pathogenicity of chlamydia abortus?

  • vary in virulence for particular hosts

  • produce disease in the respiratory, enteric, and reproductive tracts of animals and humans

4
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What is the developmental cycle of chlamydiae?

  • attachment of elementary bodies to host cells followed by receptor-mediated endocytosis

  • development of reticulate bodies, the metabolically-active replicating forms in endosomes

  • binary fission of reticulate bodies in endosome

  • condensation and maturation of elementary bodies in enlarging endosomes

  • cell lysis and release of elementary bodies, reticulate bodies and intermediate forms

5
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What is the difference between the elementary and reticulate bodies of Chlamydiae?

  • Elementary bodies: infectious extracellular

    • small, metabolically inactive

    • do not multiply, infectious

  • Reticulate bodies: non-infectious intracellular reproductive

    • large, metabolically active

    • multiply intracellularly, non-infectious

6
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What is the usual habitat of Chlamydia spp.?

gastrointestinal tract (often subclinical and persistent)

7
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How is EAE spread?

  • usually introduced into clean flocks when infected replacement ewes abort

  • shed in placentas and uterine discharges from affected ewes

  • infection occurs by ingestion

8
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True or false: Ewes infected late in pregnancy do not usually abort, but may do so in next pregnancy.

true

9
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When do ewe lambs acquire chlamydiae infection?

during neonatal period

10
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When are the first signs of chlamydial EAE infection of the placenta detectable?

day 90 of gestation

11
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What tissue does chlamydiae target?

the trophoblast layer giving rise to inflammation, thrombotic vasculitis, and tissue necrosis in the placenta

12
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How does EAE result in abortion?

reduced efficiency of fetal-maternal exchange, disruption of placental endocrine function and disruption of the immunological balance between fetus and dam

13
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What are the clinical signs of EAE?

  • abortion during late pregnancy or birth of premature weak lambs

  • necrosis of cotyledons and edema of adjacent intercotyledonary tissue in affected placentae

  • dirty pink uterine exudate

14
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How is EAE diagnosed?

  • well preserved aborted lambs, evidence of necrotic plaentitis

  • large numbers of EBs in placental smears

  • isolation of chlamydiae in suitable cell lines or in yolk sac of embryonated eggs

  • PCR, serological tests

15
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How is chlamydiae treated?

long-acting oxytetracycline to in-contact pregnant ewes to increase number of live-born lambs, but it does not eliminate the infection and treated ewes may shed chlamydiae at parturition

16
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How is EAE controlled for?

  • isolation for 2-3 weeks

  • live attenuated and inactivated vaccine

17
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What is the general morphology of the corynebacterium species?

  • small, gram-positive, catalase-positive, non-spore forming facultative anaerobes

  • pleomorphic: coccoid, club, and rod shaped

18
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Most pathogenic corynebacterium members are ____ positive.

urease

19
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Many corynebacterium members are _______ on mucous membranes.

commensals

20
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What is the difference between corynebacterium pseudotuberculosis and renal colonies?

P: small white colonies with late hemolysis

R: small to medium sized yellowish colonies with no hemolysis

21
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What change happens in older cultures of corynebacterium renal?

more pronounced pleomorphism and coccal forms become more common

22
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What is bovine cystitis?

an inflammation of the urinary bladder of cattle that may ascend the ureters to cause infection of the kidneys (pyelonephritis)

23
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What member of the Corynebacterium renal group causes the most severe form of cystitis?

C. cystitis

24
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Where is C. resale isolated from?

vulva, vagina, and prepuce of apparently normal cattle

25
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What are the contributing factors to a C. renale infection?

  • stresses of parturition

  • peak lactation

  • high-protein diet (increases pH of urine)

26
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What are the clinical signs of bovine pyelonephritis?

  • passage of blood-stained urine in otherwise normal cow

  • fever and anorexia

  • decreased milk production

  • restlessness and kicking at abdomen indicated renal pain

  • dysuria, an arched back and blood-tinged urine

  • excessive renal damage

27
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How is bovine pyelonephritis diagnosed?

  • clinical signs

  • thickened ureters and enlarged kidneys (rectal palpation

  • RBCs and protein in urine

  • culture of C. renal from urinary deposits, in association with clinical signs, is confirmatory

28
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How is bovine pyelonephritis treated?

antibiotic therapy based on susceptibility testing early in course of the disease, penicillin

29
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What pathogen causes ulcerative balanophosthitis?

Corynebacterium renale

30
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How does high protein intake and C. renal cause disease?

when protein intake is high, urinary urea concentration increases. hydrolysis of urea by C. renal results in local production of large quantities of ammonia, which is believed to irritate the penis, lamina interna of the prepuce, and skin surrounding the preputial orifice

31
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What are the clinical signs of ulcerative balanoposthitis (pizzle rot)?

  • swelling of the prepuce, swelling and inflammation interfere with urination → straining

  • ulceration around the preputial orifice, with brownish crust developing over the lesion

  • total occlusion of the preputial orifice may result

32
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How is ulcerative balanoposthitis treated and controlled?

  • isolation of affected animals and remove high-protein diet

  • clipping and cleaning hair around prepuce

  • penicillins and cephalosporins

  • testosterone treatment and limiting dietary protein