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Y3 Repro and Endo Pathology > Pathology of the reproductive tract 2 > Flashcards

Pathology of the reproductive tract 2 Flashcards

1
Q

Why is the gravid uterus more prone to infection than the non-gravid uterus?

A
  • Influence of persistent progesterone stimulation
  • Chorionic epithelium secretes substances that predispose the gravid uterus to infection
  • Placenta and embryo and immuno-privileged sites so are not directly protected by the maternal immune system
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2
Q

Name three bacterial causes of abortion

A
  • Brucella abortus (notifiable)
  • Campylobacter
  • Chlamydia abortus
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3
Q

Describe the gross effects of Brucella abortus

A
  • Oedema of foetal membranes
  • Necrotic cotyledons (soft, yellow-grey, brown exudate)
  • Thickened intercotyledonary membranes with yellowish, gelatinous fluid
  • Foetuses with serosanguinous fluid in subcutaneous tissue and body cavities
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4
Q

Describe Camplyobacteriosis in cattle

A

Necrotic cotyledones (= brucellosis)

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5
Q

Describe Camplyobacteriosis in sheep

A

Late term abortions

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6
Q

Describe chlamydiosis in sheep and goats

A
  • Late abortions, premature lambing
  • Immunity to further abortions after first
  • Foetuses and cotyledones = brucellosis
  • Can be stained with modified Ziehl-Neelsen
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7
Q

Name two protozoal causes of abortions

A
  • Neospora caninum

- Toxoplasma gondii

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8
Q

Describe the effects of Neospora caninum

A
  • Cattle
  • Mid to late gestation (3-9 months)
  • Aborted foetus
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9
Q

Describe the macro and microscopic appearance of Neospora caninum

A
  • No macroscopic alterations

* Microscopically - focal non-suppurative (no neutrophils) encephalitis, myocarditis +/- protozoal cysts.

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10
Q

Describe the effects of Toxoplasma gondii

A
  • Sheep, goats
  • Late in gestation
  • Aborted foetus
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11
Q

Describe the macro and microscopic appearance of Toxoplasma gondii

A
  • Macroscopic - usually without any alterations

* Microscopically - focal non-suppurative encephalitis +/- necrosis in other tissues

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12
Q

How does Toxoplasma gondii appear grossly

A

Placenta: bright red cotyledones with multiple, 1-3 mm, yellow-white foci scattered among the cotyledons
(Severe acute necrotising placentitis)

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13
Q

Name some viral causes of abortions

A
  • Bovine viral diarrhoea virus
  • Border disease virus
  • Equine herpes virus 1
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14
Q

How does BVDV affect pregnancy in the 1st trimester?

A

Abortion or mummification

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15
Q

How does BVDV affect pregnancy after the 1st trimester?

A

Congenital defects - the fetus is infected with BVDV

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16
Q

Describe the signs/effects on a foetus born infected with BVDV

A
  • +/- Cerebellar hypoplasia
  • Por/hydrancephaly
  • Microencephaly
  • Hypomyelination
  • Retinal atrophy
  • Optic neuritis
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17
Q

Describe Por/hydrancephaly

A

Induced by a virus in the brain that causes a focal area of necrosis, these areas become flooded with fluid and they expand.
In severe cases a large part of the neural parenchyma is replaced with fluid – can look similar to hydrocephalus

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18
Q

Describe how border disease virus affects pregnancy

A
  • Ovine pestivirus – closely related to BVDV.

- Causes similar reproductive disease in sheep as BVDV in cattle i.e. abortion on infection early in gestation.

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19
Q

Describe the congenital defects caused by border disease virus

A

Hypomyelinogenesis and growth of hair instead of wool

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20
Q

‘Hairy shakers’ occur due to which agent?

A

Border disease virus

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21
Q

Describe the effects of Equine herpes virus 1 on pregnancy

A
  • Important cause of pregnancy failure in mares (also causes respiratory and CNS disease in horses)
  • Infection of arteriolar endothelial cells leads to the virus entering placenta then fetus
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22
Q

Describe foetal lesions due to Equine herpes virus 1

A

Severe pulmonary and systemic oedema, multifocal hepatic necrosis

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23
Q

Name 3 porcine reproductive viruses

A
  • Porcine parvovirus
  • Porcine Reproductive and Respiratory Syndrome (PRRS) virus
  • Porcine circovirus 2
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24
Q

Describe how porcine parvovirus affects a foetus

A

Important cause of SMEDI (stillbirth, mummification, embryonic death, infertility) fetal death and mummification.

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25
Q

Why are foetuses affected by parvoviruses?

A

Parvoviruses can only complete their life cycle in rapidly dividing cells which is why it affects a developing foetus

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26
Q

Which virus induced abortion secondary to umbilical arteritis?

A

Porcine Reproductive and Respiratory Syndrome (PRRS) virus

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27
Q

Which virus replicates in fetal lymphoid tissues and causes death?

A

Porcine circovirus 2

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28
Q

Name 3 causative agents of vaginitis/vulvitis

A

Bovine herpesvirus-1
Equine herpesvirus-3
Trypanosoma equiperdum

29
Q

Which conditions are caused by bovine herpes virus?

A
  • Infectious bovine Rhinotracheitis
  • Infectious pustular vulvovaginitis
  • Blanoposthitis
30
Q

Describe the gross and histological appearance of BHV 1 infection

A
  • Multifocal to coalescing necrotising lesions on the mucosal aspect of the proximal vagina.
  • Herpes virus = DNA virus – replicate in the nucleus of cells. Can see large intranuclear inclusion bodies
31
Q

Describe necrotising vaginitis and vulvitis and name the agent

A

Due to secondary infection of deviated tissue (previous trauma due to difficult delivery)
Fusobacterium necrophorum

32
Q

Name 3 tumours of the vagina

A
  • Leiomyoma
  • Fibroma
  • Transmissible venereal tumour
33
Q

Describe a vaginal leiomyoma

A

Most often in middle-aged bitches – benign
Single or multiple
Derived from smooth muscle cells of vaginal wall

34
Q

Describe the features of a transmissible venereal disease

A
  • Bitch / dog (jackal, coyote, fox)
  • Rare – 1o areas where there is a feral dog population
  • Venereal transmission
  • It is the neoplastic cells themselves that are transmitted
  • Rapid growth, occasionally metastatic but spontaneous regression usual within 6 months
35
Q

Mastitis = ?

A

Inflammation of the mammary gland usually response to invasion of the gland by microbes

36
Q

What are the routes of invasion into the mammary gland?

A
  • Through teat canal (= usual route)
  • Haematogenous (tuberculosis, brucellosis)
  • Percutaneous (complication of local skin lesions)
37
Q

How is mastitis most commonly diagnosed?

A

microbiological culture of milk/exudate is most more efficient than histopathology

38
Q

There is a predisposition of dairy cows to mastitis for what reason?

A

High incidence of trauma to orifice, sphincter, streak canal of teat

39
Q

Describe the structures of the treat and streak canal

A

• Lined by stratified squamous epithelium
• Partially occluded by coagulum (natural barrier), consisting of …
- Keratin-like material from epithelial lining
- Waxy component of milk
• Trauma may cause breakdown of barrier

40
Q

Resistance to mastitis caused by … decreases with age

A

Streptococcus agalactiae

41
Q

Resistance to mastitis caused by … does not decrease with age

A

Staphylococcus aureus

42
Q

Describe the agents and effects of streptococcal mastitis

A
  • Strep. agalactiae (mammary gland as natural, sole habitat)
  • Entry via teat canal
  • Usually permanent mastitis (organism persists)
  • Organisms invade epithelium -> acute purulent inflammation, then chronic inflammation with fibrosis.
43
Q

Describe the agents of Staphylococcal mastitis

A
  • Predominantly in younger cattle

- Staph. aureus, Staph. intermedius, Staph. hyicus

44
Q

Describe the gross features of Staphylococcal mastitis

A

Gangrenous mastitis
• Usually affecting teat + adjacent portions of udder
• Tissue becomes blue, insensitive + cold
• Sloughing / separation of affected areas after ~ one week

45
Q

Name the primary agent of Coliform “toxic” mastitis in cattle

A

E.coli

46
Q

Name some secondary agents of Coliform “toxic” mastitis in cattle

A

Enterobacter, Klebsiella, Citrobacter, Serratia, Proteus (part of environmental flora; infection -> level of environmental exposure; milk derived infection)

47
Q

Describe the gross effects of Coliform “toxic” mastitis in cattle

A
  • Lesions induced by endotoxins (injury to microvasculature of alveolar walls + interstitium)
  • BLOODY DISCHARGE
  • Macroscopic: Massive oedema, haemorrhage
  • Damage to blood vessels may be so extensive that serum oozes through the surface of the udder skin, as well as into the mammary gland
48
Q

Describe the histological appearance of Coliform “toxic” mastitis in cattle

A
  • Necrosis of epithelium, oedema of septal tissue
  • Extensive necrosis of tissue maybe seen after some days
  • Sequestration is frequent if the animal survives
  • Infiltrating inflammatory cells into mammary acini + milk ducts with tissue necrosis.
49
Q

Name the agent that causes summer mastitis

A

Trueperella pyogenes

50
Q

Summer mastitis causes sporadic acute mastitis due to?

A
  • Penetrating injury
  • Contamination by flies attracted to pre-existing teat lesions
  • Infection via teat canal
51
Q

Which cows are mostly affected by Summer mastitis?

A

Mainly affecting immature + non-lactating glands of animals in pasture (dry cows)

52
Q

Describe the gross infections of summer mastitis

A

Necrotising suppurative galactophoritis with abscess formation

53
Q

What are the causative agents of mastitis in sheep?

A

i) Staph. aureus – early in lactation -> chronic granulomatous mastitis.
ii) Pasteurella haemolytica – late in lactation -> necrotising mastitis.

54
Q

Which spp are most affected by mammary tumours?

A

Most frequent tumours in bitches, third most frequent tumours in queens, rare in other species

55
Q

Describe myoepithelial cells

A
  • Continuous layer around teat sinus and ducts, discontinuous layer around acini
  • Secrete mucinous ground substance
56
Q

What is the prognosis of mammary tumours in dogs?

A
  • Percentage malignant of total removed: 30-40%
  • Mean survival time (malignant tumours): 4-17 months
  • Tumour type is important prognostic factor
57
Q

What is the prognosis of mammary tumours in cats?

A
  • Percentage of malignant to total removed: > 80%

- Carcinomas: strong tendency of local recurrence and metastasis

58
Q

What are some poor prognostic factors in cats and dogs for mammary tumours?

A
  • Age
  • Diameter of primary tumour
  • Necrosis
  • Incompleteness of surgical excision
  • High mitotic rate
  • Invasive growth
  • Presence of tumour-infiltrating lymphocytes
  • Metastasis
59
Q

Compare simple and complex adenomas

A 
Simple adenoma (simple = one cell type) - composed of well-differentiated luminal epithelial or myoepithelial cells (rare)
Complex adenoma (complex = two cell types) - composed of well-differentiated luminal epithelial and myoepithelial cells (common)
60
Q

A benign mixed mammary tumour contains which components?

A

Epithelial components and mesenchymal components (cartilage and/or bone and/or fat)

61
Q

Name and describe the most malignant mammary tumour

A

Anaplastic carcinoma

- Highly infiltrative carcinoma of pleomorphic epithelial cells, not classifiable in one of the other categories

62
Q

Name the 2 benign mammary tumours of a cat

A 
Simple adenoma (rare)
Complex adenoma (rare)
63
Q

Name 3 malignant mammary tumours of a cat

A
  • Non-infiltrating (in situ) carcinoma (rare)
  • Tubulopapillary carcinoma
  • Solid carcinoma
64
Q

Name the hormonal mammary change of cats

A

Feline mammary hypertrophy (and hyperplasia) (= fibroadenomatous change)

65
Q

Describe feline mammary hypertrophy

A

Hormonally induced proliferation of primarily intralobular ducts within a proliferative oedematous, fibrous stroma

  • Non-encapsulated
  • One or several mammary glands
  • Benign, often rapid growth
66
Q

Feline mammary hypertrophy is under the influence of?

A

Progesterone

67
Q

Which cats are most affected by feline mammary hypertrophy

A

In progesterone-treated, pregnant and very young cats (associated with exogenous and endogenous progesterone)

68
Q

How can feline mammary hypertrophy be treated?

A

Ovariohysterectomy, termination of pregnancy or progesterone treatment

Y3 Repro and Endo Pathology (5 decks)

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