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Path review > Rat Pathology Review > Flashcards

Rat Pathology Review Flashcards

1
Q

Transmission of Rat Virus

A
  • Direct (oronasal) contact
  • Urine
  • feces
  • oropharynx secretions (on fomites)
  • milk
    –(contaminated bedding was able to infect and seroconvert rats even after 5 weeks)
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2
Q

Which rat parvovirus is the only strain to produce natural disease?

A

Rat virus (RV; Kilham’s rat virus

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3
Q

Features of Rat virus

A

Parvovirus, ssDNA

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4
Q

Rat Virus causes what clinical signs/issues in pregnant females?

A
  • infertility
  • fetal resorption
  • abortion
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5
Q

T/F Pups infected w/ Rat virus in-utero will clear the infection

A

False, they will be persistently infected

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6
Q

Where can Rat Virus be found in persistently infected rats?

A

Lymphoid tissues, endothelium, vascular muscle, and renal tubule epithelium

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7
Q

Diagnosis of Rat Virus

A
  • Serology
  • PCR for DNA in tissue, feces, or environment
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8
Q

Rat Virus Pathogenesis

A
  • Infects cells in S-Phase (dna synthesis) of cell cycle
  • Attacks endothelial cells and megakaryocytes (think hemorrhage)
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9
Q

Which phase does Rat Virus infect cells?

A

S-Phase (DNA synthesis)

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10
Q

How does Rat Virus cause damage?

A

Attacks endothelial cells and megakaryocytes

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11
Q

Which rats spp. are susceptible to Rat Virus

A
  • Athymic nude rats are more susceptible
  • Immunocompetent rats can prevent clinical infection
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12
Q

Gross Lesions of Rat Virus

A
  • Congestion of lymph nodes, loss of body fat, and ***scrotal hemorrhage with fibrinous exudate
  • ***Disseinated foci of hemorrhage in cerebrum and cerebellum (both white and gray matter)
  • multifocal coagulative necrosis and hemorrhage (infarcts) in testes and epididymis
  • ***Cerebellar hypoplasia in neonatal or infant rats
  • Icterus 2° to liver damage
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13
Q

Histopathological lesions of Rat Virus

A
  • ***multifocal coagulative necrosis and hemorrhage (infarcts)
  • focal to multifocal *hepatocellular necrosis, cerebral and cerebellar necrosis
  • Intranuclear inclusions in hepatocytes, Endothelium, bile duct epithelium
  • Peliosis hepatitis, nodular hyperplasia, portal scarring are seen in rats that survive disease
  • cerebellar hypoplasia
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14
Q

Pathognomonic lesions of Rat Virus

A

Gross:
- **scrotal hemorrhage with fibrinous exudate
- **Disseinated foci of hemorrhage in cerebrum and cerebellum (both white and gray matter)
- ***Cerebellar hypoplasia

Histo:
- ***multifocal coagulative necrosis and hemorrhage (infarcts)
- focal to multifocal *hepatocellular necrosis, cerebral and cerebellar necrosis

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15
Q

Research impact of Rat Virus

A
  • impact on breeding rats
  • Attacks mitotically active cells
  • tropism for T-cells can impact immune responses to the experimental treatment or other diseases
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16
Q

Which paroviruses only produce subclinical disease in immunocompetent rats?

A
  • H-1 Virus (Toolan’s H-1 Virus)
  • Rat parvovirus
  • Rat Minute Virus
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17
Q

Features of Sendai Virus

A

Respirovirus of paramyxoviridae family (-ssDNA)

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18
Q

Transmission of Sendai Virus

A

???

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19
Q

Clinical signs of Sendai Virus

A
  • usually subclinical
  • CS varies based on immune function of individual strains
  • most pulmonary dz affects the bronchioles
  • repro issues (reduced litter size, slow growth)
  • IgG development coincides w/ clearance of respiratory tract infection and recovery of viral infection
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20
Q

Diagnosis of Sendai Virus

A
  • ***PCR from Trachea or lung samples
  • MFI or MFIA serology
  • combination of antibody-detection and presence of histopatholgical lesions (can guide dx, but is not pathognomonic)
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21
Q

Histopathological lesions of Sendai Virus

A
  • rhinitis with epithelial necrosis
  • Hyperplastic to supperative bronchitis and focal alveolitis
  • Lymphoplasmacytic cuffing may persist for months after infection
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22
Q

Susceptible rat strains to Sendai Virus

A

Brown Norway and LEW rats

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23
Q

Prevention and Control of Sendai Virus

A
  • Regular and periodic serological screening
  • If present in colony:
    — do not add any antibody-naïve rats
    — Cull any preg. And preweanling rats, halt breeding
    — virus should be eliminated in 4-8 weeks
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24
Q

Research Impact of Sendai Virus

A
  • Any respiratory research might be affected
  • May impact immune responses to research target
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25
Q

Features of Sialodacryoadenitis virus (RCV-ADA)

A
  • Coronavirus
  • +ssRNA (tends to mutate more frequently than DNA)
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26
Q

Transmission of Sialodacryoadenitis virus

A
  • Direct contact (nasal secretions, saliva)
  • Aerosols
  • Fomites
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27
Q

Do different coronaviruses provide protection against others?

A

No. Reinfection by same strain also possible, but CS less severe

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28
Q

Clinical signs of Sialodacryoadenitis virus

A
  • ** Cervical or intermandibular swelling, sniffling, blepharospasm, epiphora, and nasal and lacrimal discharges
    -Chromodacryorrhea (not specific for rat coronavirus)
  • Repro problems: irregular cycling, small litters, neonatal mortality
  • may produce resp. dz in young rats (rhinitis, tracheitis, pneumonia)
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29
Q

Morbidity / mortality of Sialodacryoadenitis virus

A

high morbidity / low mortality

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30
Q

Diagnosis of Sialodacryoadenitis virus

A
  • MFIA serology
  • PCR from affected glands
  • Histopath can be helpful in CLINICAL cases
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31
Q

Which strains are susceptible to Sialodacryoadenitis virus?

A
  • Athymic nude rats: develop chronic persistent infections and wasting disease
    — significant additive effects in rats prev. exposed to Mycoplasma pulmonis and Filobacterium rodentium (CAR bacillus (see below)
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32
Q

Gross lesions of Sialodacryoadenitis virus

A
  • **Swelling of the submandibular and parotid salivary glands with edema
  • Regional lymph node enlargement
  • Unilateral or bilateral glaucoma Megaglobus, hyphema, and corneal ulceration
  • Chromodacryorrhea
  • Rhinitis
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33
Q

Histopath lesions of Sialodacryoadenitis virus

A
  • Salivary and lacrimal glands:
    — necrosis of salivary and lacrimal ducts; edema w/ mixed inflammation
  • Respiratory epithelium:
    — loss of cilia and mucosal necrosis; edema, inflammation, fibrinocellular exudates; epithelial hyperplasia (tracheitis, focal bronchitis, and bronchiolitis)
    — necrotizing rhinitis w/ mixed inflammation.
  • ophthalmic lesions:
    — Keratitis/KCS; anterior uveitis and Glaucoma w/ retinal degeneration
  • Reparative stage:
    — Squamous metaplasia of salivary, Harderian, and lacrimal glands w/ mixed inflammation; reactive hyperplasia of cervical LNs 7-10 d. post exposure
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34
Q

Describe the Two stages of Sialoacryoadenitis virus

A

Acute Stage:
Virus infects epithelial cells in salivary and lacrimal glands, causing necrosis of ductular structures spreading to adj. acini and effacement of normal architecture (**mucous salivary glands (sublingual Salivary glands) not affected)

Reparative Stage:
Nonkeratinizing Squamous metaplasia of ductal and acinar structures of salivary and lacrimal glands takes place with reactive hyperplasia of cervical lymph nodes

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35
Q

Prevention of Sialodacryoadenitis virus

A

Prevention:
- know pathogen status of vendor
- Effective quarantine programs
- keep separate from wild rats

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36
Q

Control of Sialoacryoadenitis virus

A

Control:
- (6-8wks):
– allow infection to spread so that whole colony seroconverts
– keep infected colony isolated
– suspend breeding and remove preweanlings from colony

OR

– separate seropositive breeders from original colony
– Allow both original and seropositive groups to breed separately
– depop. The original and replace w/ the seropositive group once the seropositive breeders are in late gestation

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37
Q

Research Impacts of Sialodacryoadenitis virus

A
  • Any studies interested in examining tissues from affected sites (period of active infection and 2-3w. of reparative period; ocular lesions may be long-term)
  • decreased food intake
  • decr. Salivary gland production of EGF, affecting carcinogenicity studies and possibly repro.
  • damage to olfactory and vomeronasal organ epithelium -> may affect pheromone detection -> may affect breeding
  • unanticipated complications (impairment of nerve regeneration)
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38
Q

Features of Polyomavirus

A
  • small dsDNA polyomavirus
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39
Q

Clinical signs of rat polyomavirus

A
  • ***wasting, nonsuppurative sialoadenitis, dyspnea, and interstitial pneumonia
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40
Q

Rat Strains susceptible to Rat Polyomavirus

A
  • Athymic nude rats susceptible
  • Euthymic rats NOT susceptible
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41
Q

Histopathological lesions of rat Polyomavirus

A
  • Large intranuclear inclusions in duct epithelium of salivary glands, less frequently in salivary acini, bronchiolar epithelium, and alveolar lining cells (“relatively diagnostic”)
    (“pushes normal DNA to edge”)
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42
Q

Features of Rotavirus

A

Group B rotavirus, dsRNA, possibly of human origin

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43
Q

Transmission of Rat Rotavirus

A

-Fecal oral (feces and fomites)

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44
Q

Clinical signs of Rat Rotavirus

A

-** diarrhea within 24-36 hours
- slowed growth

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45
Q

Gross lesions of rat rotavirus

A
  • milk curd in stomach (indicates presence of appetite)
  • watery contents in proximal sm. Intestine
  • yellow-brown to green fluid and gas in distal sm. Intestine and lg. intestine
  • Erythema and bleeding of the perianal skin
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46
Q

Histopath lesions of rat rotavirus

A
  • **Pathognomonic epithelial syncytia w/ variably present eosinophilic intracytoplasmic inclusions
  • Intestinal villus attenuation, necrosis of enterocytes
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47
Q

What is the biggest concern for Cowpox virus

A

The zoonotic potential

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48
Q

Features of Cowpox virus

A
  • orthopoxvirus, dsDNA
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49
Q

Clinical signs of cowpox virus

A

CS may vary:
- may be subclinical
-proliferating and necrotizing circular dermal lesions
- Acute pulmonary form w/ high mortality (intranasal inoculation leads to peracute mortality)

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50
Q

Morbidity/mortality of cowpox virus

A

Enzootic among rodents;
(humans, cattle, felids, and some other mammals susceptible)

High mortality w/ acute pulmonary form

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51
Q

Gross lesions of cowpox virus

A

Dermal lesions
- Proliferative and necrotizing lesions on libs, tail, tongue, nose, inguinal skin (mostly non-haired skin)
- tail amputation

Pulmonary lesions:
- Focal necrotizing lesions in mucosa
- Pulmonary congestion and edema

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52
Q

Histopath lesions of cowpox virus

A
  • Hyperplasia and necrosis of epithelium
  • bronchointerstitial pneumonia, congestion, eema
  • large eosinophilic intracytoplasmic inclusion bodies (Guarnieri bodies)
  • Lymphoid necrosis
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53
Q

Features of Rat Cytomegalovirus

A
  • Beta-herpesvirus
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54
Q

Clinical signs of rat cytomegalovirus

A

often subclinical

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55
Q

Pathogenesis of rat cytomegalovirus

A
  • Infects salivary and lacrimal glands
  • Cytomegaly w/ intracytoplasmic and intranuclear inclusions in ductal epithelium
  • nonsuppurative interstitial inflammation
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56
Q

Rat strains susceptible to Rat Cytomegalovirus

A

not really seen in lab rats, common in wild rats

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57
Q

Features of Rat Theilovirus

A

Cardiovirus genus

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58
Q

transmission of Theilovirus

A

Fecal-oral

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59
Q

Clinical signs of Theilovirus

A

Often subclinical

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60
Q

Diagnosis of rat Theilovirus

A

Serology

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61
Q

Pathogenesis of Rat Theilovirus

A

¬Replicates in small intestinal enterocytes; shed in feces for 4-8 weeks

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62
Q

Rat Strains susceptible to Rat Theilovirus

A

Nude rats: infection leads to Persistent shedding, virus found in intestines and elsewhere

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63
Q

Gross and histopath changes of Rat Theilovirus

A

No gross or histopath changes

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64
Q

Control/prevention of Rat Theilovirus

A

Control via test and cull

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65
Q

Features of Pneumonia Virus of Mice (PVM)

A
  • Pneumovirus of paramyxoviridae family
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66
Q

Clinical signs of Pneumonia Virus of Mice

A

subclinical infection

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67
Q

Pathogenesis/concerns of Pneumonia Virus of Mice

A

** possibly a significant co-pathogen w/ Mycoplasma pulmonis

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68
Q

What species does pneumonia virus of mice infect?

A

Infects mice, rats, hamsters, gerbils, guinea pigs, and rabbits

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69
Q

Histopath lesions of Pneumonia Virus of Mice

A

Vasculitis, interstitial pneumonitis w/ necrosis

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70
Q

Primary concern of Hantavirus

A

ZOONOTIC

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71
Q

What are the human diseases associated with hantavirus

A

(Seoul Hantavirus causes hemorrhagic fever w/ renal syndrome in humans); (hantavirus pulmonary syndrome in Florida)

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72
Q

Features of hantavirus

A

Bunyaviridae family

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73
Q

Clinical signs of Hantavirus

A

Chronic, subclinical infection

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74
Q

T/F Rodents are not natural reservoirs for Hantavirus

A

False, they are

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75
Q

Transmission of Hantavirus of Rats

A

virus shed in feces and urine

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76
Q

Does Rat Adenovirus cause clinical disease

A

no

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77
Q

Histopath lesions associated with Rat Adenovirus

A

Inclusions can be seen in enterocytes, typically incidental findings

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78
Q

Features of Filobacterium Rodentium

A

(formerly Cilia-Associated Respiratory (CAR) Bacillus)
- filamentous, G- argyophilic

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79
Q

Transmission of Filobacterium Rodentium

A
  • direct (oronasal) contact, usually in young (neonatal) rats
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80
Q

Severity and Clinical signs of Filobacterium Rodentium

A

Severity variable
(may be clinical, subclin., or only clinical if copathogen present)

CS:
- Oculonasal discharge, increased resp. effort, hunched posture, anorexia w/ weight loss

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81
Q

Diagnosis of Filobacterium Rodentium

A
  • PCR from nasopharyngeal or tracheal swabs
  • Serology (ELISA, MFIA, IFA)
  • ID of org. w/ silver stains (like Warthin-Starry staining)
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82
Q

Pathogenesis of Filobacterium rodentium

A
  • Colonizes cilia of airway epithelium, starting w/ upper airways and spreading to the lungs

***bacteria line the apex of the respiratory epithelium, interspersed between cilia

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83
Q

Which rat strains are susceptible to Filobacterium rodentium

A

all strains

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84
Q

Gross lesions of Filobacterium Rodentium

A
  • Purulent discharge in upper and lower airways
  • Lungs fail to collapse w/ release of pressure
  • May have cranioventral consolidation
  • Lungs may have mottled red to gray-tan appearance w/ dilated and mucus-filled airways
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85
Q

Histopath lesions of Filobacterium rodentium

A
  • Chronic suppurative bronchitis and bronchiolitis w/ bronchiectasis
  • Lymphocytes and plasma cells surrounding airways (peribronchiolar cuffing)
  • Marked leukocytic infiltration in the lamina propria of affected airways
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86
Q

Control of Filobacterium rodentium

A

Control:
- evaluate risk of wild rodent exposure
- Test and cull and/or depop-repop

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87
Q

Research impact of Filobacterium rodentium

A
  • Cannot be used for resp. research, even if asymptomatic
  • clinically sick animals are generally unfit for research
  • potential complications w/ inflammation, ciliary function, and immune modulation
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88
Q

Features of Mycoplasma pulmonis

A
  • (G-); very small
  • Lacks a cell wall entirely
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89
Q

transmission of Mycoplasma pulmonis

A
  • direct contact
  • Aerosolization
  • Transplacental
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90
Q

Which is more likely to present clinical signs: Filobacterium rodentium or Mycoplasma pulmonis

A

Mycoplasma pulmonis

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91
Q

Clinical signs of Mycoplasma pulmonis

A

CS:
- Oculonasal discharge, increased resp. effort, hunched posture, anorexia, weight loss
- Repro. Deficits

Potential for infections beyond the lungs (due to affinity for ciliated cells)
- resp. epithelium -> pneumonia
- middle ear -> otitis media
- Uterus -> endometritis
- Synovium -> arthrosynovitis (less common)

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92
Q

Diagnosis of Mycoplasma pulmonis

A
  • PCR on nasopharyngeal or tracheal swab, lung tissue, exudate
  • Culture
  • IHC
  • Serology less reliable since seroconversion takes a long time, and cross-reacts w/ other Mycoplasma spp.
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93
Q

Pathogenesis of Mycoplasma pulmonis

A

**Strong predilection for tissues w/ ciliated epithelium

Colonies cilia of airway epithelium, starting w/ upper airways and spreading to lungs (may take up to 6 mos.)

Colonize the apex of the resp. epithelium, effacing the surface with loss of cilia

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94
Q

Susceptible strains of Mycoplasma pulmonis

A

All strains

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95
Q

Gross lesions of Mycoplasma pulmonis

A

Lungs:
- purulent material within trachea and bronchi; red to gray consolidation of the lungs with *** asymmetrical cranioventral enlargement and distended/ectatic bronchi

Ears
- purulent material within tympanic bullae

Repro tract
- clear to purulent exudate within uterine horns, ovarian bursae, and oviducts

Synovium
- Swelling of tibiotarsal joints

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96
Q

Histopath lesions of Mycoplasma pulmonis

A

Lungs:
- ***loss and flattening of cilia, squamous metaplasia
- bronchial and bronchiolar neutrophilic exudate (purulent material in other organs)

  • ***Bronchiectasis and bronchiolectasis (ciliostasis -> unable to clear mucus or inflammatory exudate -> pressure expansion of airways -> bronchiectasis and bronchiolectasis
    (essentially, disruption of the ciliary elevator)
  • ***Lymphoid hyperplasia
    – intact organisms and cell membranes are superantigens and B-cell mitogens, resulting in marked peribronchiolar lymphocytic infiltration
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97
Q

Control of Mycoplasma pulmonis

A

Control:
- reputable vendors
- quarantine and screening
Prevent exposure to wild rodents
- Depop and repop

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98
Q

Research Impact of Mycoplasma Pulmonis

A
  • Impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
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99
Q

What is the Etiology of Chronic Respiratory Disease of Rats

A

Etiology:
- Mycoplasma pulmonis (the major causative agent)
- CAR Bacillus (Filobacterium rodentium)
- Sendai virus
- Rat Coronavirus (Sialodenacryoadentitis virus)
- Ammonia exposure above 25ppm

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100
Q

Features of Corynebacterium kutscheri

A
  • (G+); short rod
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101
Q

Transmission of Corynebacterium kutscheri

A
  • Predominantly fecal-oral
  • Direct contact
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102
Q

Clinical signs of Corynebacterium kutscheri

A

Frequently subclinical to inapparent (clinical dz and mortality usually ass. w/ underlying immunosuppression, nutritional deficits, etc.)

CS:
- weight loss
- resp. distress
- ruffled hair coat
- death in a few days after onset of signs

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103
Q

Diagnosis of Corynebacterium kutscheri

A

PCR or culture of
- cervical LNs, oropharynx, nasopharynx, middle ears, preputial glands, feces

Histopath w/
- Gram, Warthin-Starry, or Giemsa stains
(characteristic appearance of bacteria arranged in acute angles; referred to in textbooks as “Chinese letter-like” arrangement” (well that’s messed up)

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104
Q

Pathogenesis of Corynebacterium kutscheri

A

Carried in oropharynx and Regional LNs for weeks -> hematogenous spread to many organs

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105
Q

Strains / spp. susceptible to Corynebacterium kutscheri

A

Can infect mice, rats, and guinea pigs

Any age can be affected

Immunocompromised rats most at risk of infection

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106
Q

Gross lesions of Corynebacterium kutscheri

A
  • Red crusty lesions around eyes and nares
  • possibly mucopurulent exudate around nose
  • raised pale tan to white foci on lungs and possibly other organs
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107
Q

What is the causative agent of pseduotuberculosis

A

Corynebacterium kutscheri

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108
Q

Histo lesions of corynebacterium kutscheri

A
  • Abcesses (nodule-like lesions w/ suppurative inflammation and necrosis) in lungs an dother organs
    – predominantly lungs in rats (liver, kidneys, and lungs in mice)
  • Bacteria form large colonies within lesions
  • Inflammation often centered around blood vessels (embolic pattern of disease (e.g., embolic glomerulonephritis)
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109
Q

control of corynebacterium kutscheri

A

Control:
- depop. And repop
- Sterilization

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110
Q

Research impact of corynebacterium kutscheri

A
  • impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
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111
Q

Features of Clostridium piliforme

A
  • (G-); filamentous rod
    (other clostridium spp. Are often G+)
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112
Q

Transmission of Clostridium piliforme

A

Forms spores (can survive in the environment for up to 1 year)

  • ingestion of spores from the environment
  • fecal oral
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113
Q

Morbidity / mortality of Clostridium piliforme
(Tyzzer’s disease)

A

Low morb. / Hight mort.
(often acute death w/o any clinical signs)

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114
Q

Diagnosis of Clostridium piliforme

A
  • (G-); stains positively on silver, PAS, or Giemsa stains
  • Serology: risk of false positives, so interpret results w/ histopath
  • PCR on cecal contents or feces (less reliable since immunocompetent animals will clear the bacteria)
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115
Q

Rats strains susceptible to Clostridium piliforme

A

Affects many animal spp.
- spp.-specific variations in lesions

  • Young rats in the postweaning period more susceptible to dz
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116
Q

gross lesions of Clostridium piliforme

A
  • Small white foci throughout the liver and heart
  • ***Megaloileitis: flaccid and dilated ileum filled w/ hemorrhage
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117
Q

Histo lesions of Clostridium piliforme

A
  • Multifocal random necrotizing hepatitis
  • necrotizing myocarditis
  • necrohemorrhagic transmural ileitis w/ flaccid and dilated ileum (megaloileitis)
  • bacteria are arranged in thin bundles within cytoplasm of cells near areas of necrosis
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118
Q

pathognomonic lesions of Clostridium piliforme

A
  • Megaloileitis: flaccid and dilated ileum filled w/ hemorrhage
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119
Q

Control and prev. of Clostridium piliforme

A

Control and prev.
- keep facilities clean
- prevent exposure to wild animals (wide range of hosts and persistence of spores)

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120
Q

Research impact of Clostridium piliforme

A
  • Clinically sick animals
  • sudden death of animals, esp. young animals
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121
Q

Research impact of Streptococcus pneumoniae

A
  • Impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
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122
Q

Control of Streptococcus pneumoniae

A

Control:
- Reputable vendors
- Quarantine and screening
- Depop if indicated

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123
Q

Histo lesions of Streptococcus pneumoniae

A
  • Fibrinopurulent (fibrin, degenerate neutrophils), polyserositis, and bronchopneumonia
  • embolic neutrophilic inflammation in liver and other organs
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124
Q

Gross lesions of Streptococcus pneumoniae

A

-Fibrinous and purulent pleuritis, pericarditis, and pneumonia (possibly peritonitis, periorchitis, and meningitis

  • Fluid in trachea
  • Mucopurulent exudate in nasal passage and sometimes tympanic bullae
  • Lung consolidation
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125
Q

Rat strains/ages susceptible to Streptococcus pneumoniae

A

Young rats may develop disease

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126
Q

Diagnosis of Streptococcus pneumoniae

A
  • Nasopharyngeal culture via blood agar place, optochin inhibition test
  • PCR

Tests are best w/ histopath to corroborate, since there are nonpathogenic strains

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127
Q

Clinical signs of Streptococcus pneumoniae

A

Often subclinical
- Dyspnea
- serous to mucopurulent nasal discharge

128
Q

Transmission of Streptococcus pneumoniae

A
  • Aerosol
  • Fomites

ZOONOTIC
(humans are the natural host for this bacteria -> potential reverse zoonosis)

129
Q

Features of Streptococcus pneumoniae

A
  • (G+); diplococcus α-hemolytic
  • normal inhabitant of tympanic bullae and nasal turbinates

Formerly a major health concern but now well-controlled in lab rats

130
Q

Features of Bordetella bronchiseptica

A
  • (G-), coccobaccili
131
Q

Clinical signs of Bordetella bronchiseptica

A
  • Suppurative rhinitis w/ multifocal bronchopneumonia and peribronchial lymphoid hyperplasia (cranioventral pneumonia)
132
Q

diagnosis of Bordetella bronchiseptica

A

Must be able to isolate the bacteria in large #s for definitive dx, and look for copathogens

133
Q

Morbidity / mortality of Enterococcus

A

Epizootics of enteric dz in suckling rats w/ high morbity and high mortality

134
Q

Features of Enterococcus

A

(entercoccal enteropathy)
- (G+) cocci
- part of normal rat microbiome

135
Q

Clinical signs of Enterococcus

A
  • diarrhea, fecal staining of fur
  • stunted growth, distended abdomens
136
Q

Diagnosis of Enterococcus

A

Combo of CS w /ID of bacteria on histology

137
Q

histo lesions of enterococcus

A
  • Large #s of G+ coccoid bacteria lining otherwise normal enterocytes in the sm. intestine
138
Q

gross lesions of enterococcus

A
  • stomachs distended w/ milk (still have good appetite)
  • Dilation of small and large intestines w/ gas and fluid
139
Q

research impact of Helicobacter

A

Nothing significant as long as the animals are not clinical

140
Q

Control of Helicobacter

A

Control:
- Treat individuals or small groups w/ abx (amoxicillin, clarithromycin, metronidazole, omeprazole)

141
Q

histo lesions of Helicobacter

A

In athymic nude mice:
- Crypt hyperplasia and herniation

(If a pathogen causes a hyperplastic response (or other rapid development) that can be a primer for neoplastic development

142
Q

Gross lesions of Helicobacter

A

In athymic nude mice:
- Proliferative and ulcerative typhlitis, colitis, and proctitis

(The wall itself is thickened, not just enlarged)

143
Q

rat strains susceptible to Helicobacter

A

None are known to produce natural disease in immunocompetent rats

Experimentally, disease has been easier to produce in Brown Norway rats than SD rats

Athymic nude rats can develop dz w/ Helicobacter bilis

144
Q

diagnosis of Helicobacter

A
  • PCR on feces can screen for helicobacter (approx.. 20% of lab rats can have Helicobacter naturally)
  • Culture from feces is possible, but complicated (Helicobacter typically doesn’t culture well)
145
Q

transmission of Helicobacter

A

feces most likely

146
Q

features of Helicobacter

A
  • (G-); flagellated; spiral, curved, or straight

Many spp. ID’ed in lab animals, including several in rats

147
Q

Features of Lawsonia intracellularis

A
  • (G-) argryophlic, small, curved rod

Obligate intracellular org. that lives inside the cytoplasm of infected host’s enterocytes

148
Q

Susceptible rat strains to Lawsonia intracellularis

A

Significant dz in hamsters and rabbits, less so in rats

149
Q

gross lesions of Lawsonia intracellularis

A

Proliferative enteritis

150
Q

histo lesions of Lawsonia intracellularis

A
  • Severe mucosal hyperplasia w/ crypt herniation
  • Histiocytic to granulomatous inflammation, may form nodules in intestine or extend to mesenteric lymph nodes

Association w/ colonic adenocarcinoma

151
Q

Is Clostridium difficile a significant cause of dz in rats?

A

No, but it can cause enterotoxemia in rats under certain conditions due to toxin formation

152
Q

Features of Salmonella enterica

A

(G-) w/ wide host range

2,500+ serovars in S. enterica spp

Rare in lab animals but common in wild animals

153
Q

Clinical signs of Salmonella enterica

A

Often subclinical (think Typhoid Mary)
- nonspecific signs (lethargy, wt. loss)
- soft stools and diarrhea
- acute death

154
Q

Diagnosis of Salmonella enterica

A

PCR or Culture
- Mesenteric lymph nodes
- Repeated fecal samplings (salmonella may be intermittently present, esp. in carriers

155
Q

Pathogenesis of Salmonella enterica

A

LPS (endotoxin) and other virulence factors:
- attack host cells, evade immune cells, and are potent activators of immune response (including sepsis)

  • most damage done is by bacterial toxins, exp. By damaging blood vessels and activating clotting cascades
156
Q

Gross lesions of Salmonella enterica

A
  • Thickened and ulcerated intestines (cecum and ileum)
  • Splenomegaly
  • Multiple small, white-yellow spots on liver
  • enlarged LNs
157
Q

Histo lesions of Salmonella enterica

A
  • Ulcerated and inflamed cecum and ileum
  • Lymphoid hyperplasia and necrosis in Peyer’s patches, spleen, lymph nodes
  • Thromboemboli w/ bacteria in liver, spleen, and LNs
  • Necrosis in intestines, liver, spleen, and lymph nodes
158
Q

Control/prev. of Salmonella enterica

A
  • Reputable vendors
  • Quarantine and screening
  • Good hygiene (animals and humans)
  • Prevent exposure to wild rodents
  • Depop and deep cleaning if positive
159
Q

Research impact of Salmonella enterica

A

Zoonotic risk, do not use any animals from an infected population

160
Q

T/F Campylobacter jejuni is not zoonotic

A

false, it is

161
Q

Clinical signs of campylobacter jejuni

A

Usually subclinical

Mild diarrhea in young rats possible

162
Q

Susceptible strains of Campylobacter jejuni

A

Wide range of possible hosts (gastroenteritis in humans)

163
Q

histo lesions of Staphylococcus aureus

A
  • Coagulative necrosis of the epidermis (epidermolytic toxin?)
  • colonies of cocci
  • Hyperplasia of adjacent epidermis
  • neutrophils in acute stages, dermal fibrosis, and lymphocytes in chronic stages
164
Q

Gross lesions of Staphylococcus aureus

A
  • well-circumscribed, red, ulcerated regions over shoulder with hair loss and crust (rib cage, submandibular region, neck, ears, and head may also be affected)
165
Q

Rat strains susceptible to Staphylococcus aureus

A

— NK-cell-deficient beige rats are most susceptible, esp. males, w/ dz similar to Chediak-Higashi syndrome

166
Q

Pathogenesis of Staphylococcus aureus

A
  • Trauma w/ persistent irritation (linoleic acid involvement? -> barrier function disruption)
  • can cause ulcerative skin lesions in adult rats
    — NK-cell-deficient beige rats are most susceptible, esp. males, w/ dz similar to Chediak-Higashi syndrome
167
Q

diagnosis of Staphylococcus aureus

A

Ulcerative skin lesions w/ G+ cocci are diagnostic

Culture of coagulase-positive S. aureus

168
Q

clinical signs of Staphylococcus aureus

A

usually subclinical

169
Q

features of Staphylococcus aureus

A
  • (G+) cocci

Ubiquitous commensal bacteria of skin and mucous membranes

170
Q

features of Streptobacillus moniliformis

A
  • (G-) pleomorphic rod to filamentous bacteria

Commensal org. in nasopharynx of rats (also in blood and urine in cases of infection)

171
Q

What is the major concern of Streptobacillus moniliformis

A

ZOONOTIC
- Major concern w. this bacteria is human dz
— CS in huamns include maculopapular and pustular rash, fever, headache, and polyarthritis
— Mortality document in healthy children and adults

In Asia -> Rat Bit Fever (caused by Spirillum muris; similar CS)

Haverhill fever (caused by S. moniliformis) is a form of Rat Bite Fever
- human symptoms: resemble severe flu, but may develop meningitis and endocarditis
- Associated w/ ingestion of rat-contaminated foodstuffs, particular milk

172
Q

Transmission of Streptobacillus moniliformis

A

Transmission can occur through bites, close contact w/ infected rats, or inadvertent ingestion of rat feces/urine

173
Q

transmission of Pasteurella pneumotropica

A

Commonly carried in intestine, may colonize all other mucosal surfaces in the body

Frequently isolated from animals w/o disease and intranasal inoculation fails to produce lesions

  • Direct contact
  • Does not persist long in environment
174
Q

clinical signs of pasteurella pneumotropica

A

Mild nasal inflammation and sneezing in Athymic rats
(GI, Resp, Repro)

Important 2° or opportunistic infection in 1° Mycoplasma pulmonis or Sendai virus infections
- interstitial pneumonia with neutrophilic infiltration has been observed in pregnant rats w/ 1° Sendai virus and 2° P. pneumotropica infection -> high rate of fetal death

  • Lesions with other may include rhinitis, sinusitis, conjunctivitis, otitis media, suppurative bronchopneumonia, subcutaneous abscessation, suppurative or chronic necrotizing mastitis, and pyometra
175
Q

Research impact of pasteurella pnemotropica

A
  • No impact unless animals are clinically ill
  • No effort required to remove from colony unless immunodeficient animals are present
176
Q

transmission of Pseudomonas
aeruginosa

A
  • Opportunistic pathogen
  • Environmental contaminant common in soil, water, or sewage (most frequently from human handling with unwashed/ungloved hands)
  • biofilms make treatment and prevention difficult (resists many chemical cleaning treatments)
177
Q

clinical signs of Pseudomonas
aeruginosa

A

Acute lesions are consistent with septicemia from other (G-) bacteria (pulmonary edema, splenomegaly, visceral ecchymoses, vegetative endocarditis)

Chronic stage of dz:
- multifocal necrosis and abscesses may be present in organs such as lung, spleen, and kidneys
- Pulmonary thromboemboli, bacteria and hemorrhage in alveoli

178
Q

diagnosis of Pseudomonas
aeruginosa

A

Dz requires repeated/continuous exposure and some other factors including:
- irradiation, steroids, or other immunosuppressant treatments (neutropenia is a large risk factor)
- surgical procedures such as indwelling jugular catheter placement

179
Q

research impact of Pseudomonas
aeruginosa

A

Depends on studies using these techniques

180
Q

Transmission of Mycoplasma muris

A
  • transmitted primarily by Polyplax spinulosa
181
Q

clinical signs of Mycoplasma muris

A
  • natural infections are invariably inapparent, w/ mild transient bacteremia, splenomegaly, and erythrocytic reticulocytosis
  • splenectomy causes hemolytic anemia w/ hemoglobinuria and death
  • Corticosteroids DO NOT activate subclinical infections
182
Q

Is Klebsiella pneumoniae zoonotic

183
Q

clinical signs of Klebsieall pneumoniae

A

Minimal inflammation, typically a nonpurulent interstitial nephritis

Rats important as carriers

184
Q

Causes of hepatic necrosis in rats

A
  • Bacterial: Clostridium piliforme, Corynebacterium kutscheri)
  • Viral: rat virus (parvovirus)
185
Q

Transmission of Pneumocystis
carinii

A
  • Aerosol
  • possibly fomites
186
Q

clinical signs of Pneumocystis
carinii

A

Dyspnea
Cyanosis
Weight loss

187
Q

diagnosis of Pneumocystis
carinii

A

Special stains

PCR of lung tissue, bronchiolar lavage, or oral swabs

Serology 6-8 wks after infection

188
Q

Pathogenesis of Pneumocystis
carinii

A

In immunodeficient rats:
- interstitial pneumonia with histiocytes (varying in severity)
- Typically, **lots of histiocytes within the airways
- **pink, foamy material within alveoli
— the “foam” are trophozoites
— yeast-like cysts are larger (3-5µm) and less common

In immunocompetent rats:
- transient lymphocytic pneumonia around blood vessels and bronchioles, similar to viral disease (previously thought to be rat respiratory virus)
- far fewer organisms than in immunodeficient rats

189
Q

Gross lesions of Pneumocystis
carinii

A
  • lungs fail to collapse
  • fel small pale tan or white foci on lung surface
190
Q

Histo lesions of Pneumocystis
carinii

A
  • interstitial pneumonia with neutrophils and histiocytes
  • Very high numbers of intra-alveolar histiocytes
  • lymphocytes around airways
191
Q

Research impact of Pneumocystis
carinii

A

Unknown w/ immunocompetent rats

Possible impact for inhalation/anesthesia studies

192
Q

Features of Trichophyton mentagrophytes

A

(Dermatophytosis, aka Ringworm)
- most common dermatophyte of rats, mice, rabbits

193
Q

Transmission of Trichophyton mentagrophytes

A

More common in wild and pet rats

Direct contact, fomites

ZOONOTIC

194
Q

diagnosis of Trichophyton mentagrophytes

A

Special stains w/ fungi on hair shafts

Fungal culture

Skin-scrapings

195
Q

gross lesions of Trichophyton mentagrophytes

A
  • patchy hair loss
  • erythematous to pustular lesions
196
Q

Histopath lesions of Trichophyton mentagrophytes

A

Hyperkeratosis, epidermal hyperplasia, leukocytic dermatitis and folliculitis

197
Q

clinical signs of Aspergillus

A

Chronic rhinitis w/ fungal hyphae

198
Q

research impact of aspergillus

A

Potential for lung involvement

199
Q

Gross lesions of Blastomyces
dermatiditis

A
  • Gray-white lung nodules
  • Bronchopneumonia w/ pyogranulomas
  • thick-walled yeast forms
200
Q

Which spp. does encephalitozoon cuniculi affect typically

A

primarily a disease of rabbits

201
Q

Features of Cryptosporidium

A
  • intracellular parasite of intestinal epithelial cells (present within the cell but not the cytoplasm)
202
Q

Clinical signs of Cryptosporidium

A

Transient and mild disease in immunocompetent animals

203
Q

Rat strains susceptible to Cryptosporidium

A

Immunosuppressed or athymic rats may be susceptible to clinical disease

Outbreak of diarrhea and high mortality among infant rats in Rapp hypertensive strain

204
Q

Features of Syphacia muris

A

Round esophageal bulb, small cervical alae

♀ - 2.8-4.0mm long, vulva in anterior ¼ of body
♂- 1.2-1.3mm long, tail is long and pointed

Ova
72-82x25-36µm
Thin-shelled, ellipsoidal, flattened on one side

Complete direct lifestyle 7-8d.

205
Q

Features of Syphacia obvelata

A

Round esophageal bulb, small cervical alae

♀ - 3.4-08mm long, vulva in anterior 1/6 of body
♂- 1.1-1.5mm long, tail is long and pointed

Ova
118-153 x 33-55µm
Thin-shelled, Banana-shaped

Complete direct lifestyle 11-15d.

206
Q

Features of Aspiculuris tetraptera

A

Oval esophageal bulb
Prominent cervical alae end abruptly at level of esophageal bulb

♀ - 2.6-4.7mm long, vulva in anterior ¼ of body
♂- 2.0-4.0mm long, tail is blunt and conical

Ova
89-93 x 36-42µm
Morulated and football-shaped

Complete direct lifestyle 23-25d.

207
Q

Transmission of Syphacia
muris

A

Fecal-oral
Fomites
Contaminated water

208
Q

Transmission of Syphacia
obvelata

A

Fecal-oral
Fomites
Contaminated water

209
Q

Transmission of Aspiculuris tetraptera

A

Fecal-oral
Fomites
Contaminated water

210
Q

Clinical signs of Syphacia
muris

A

Usually subclinical, but severe infestations w/ high numbers elicit clinical disease in young rats

CS: Diarrhea, rectal prolapse, failure to gain weight, impaction, intussusception

211
Q

Clinical signs of Syphacia
obvelata

A

Usually subclinical, but severe infestations w/ high numbers elicit clinical disease in young rats

CS: Diarrhea, rectal prolapse, failure to gain weight, impaction, intussusception

212
Q

Clinical signs of Aspiculuris tetraptera

A

Usually subclinical, but severe infestations w/ high numbers elicit clinical disease in young rats

CS: Diarrhea, rectal prolapse, failure to gain weight, impaction, intussusception

213
Q

Diagnosis of Syphacia
muris

A

Maceration of cecum/colon with examination under stereomicroscope**
- most effective

ID of worms in large intestine (histopathology)

Touch tape

Fecal flotation, fecal concentration and centrifugation for eggs

PCR testing

214
Q

Pathogenesis of Syphacia
muris

A

Direct life cycles
- eggs are deposited in colon or perianal area
- eggs embryonate and become infectious
- new hosts become infected by ingestion of eggs in contaminated food or water or fomites (or direct migration of larvae from the anus to the colon (autoinfection))

215
Q

Pathogenesis of Syphacia
obvelata

A

Direct life cycles
- eggs are deposited in colon or perianal area
- eggs embryonate and become infectious
- new hosts become infected by ingestion of eggs in contaminated food or water or fomites (or direct migration of larvae from the anus to the colon (autoinfection))

216
Q

Diagnosis of Aspiculuris tetraptera

A

Maceration of cecum/colon with examination under stereomicroscope**
- most effective

ID of worms in large intestine (histopathology)

TOUCH TAPE DOES NOT WORK FOR ASPICULURIS

Fecal flotation, fecal concentration and centrifugation for eggs

PCR testing

217
Q

Treatment/control of Syphacia
obvelata

A
  • anthelmintic tx (fenbendazole, ivermectin, new generation avermectins, levamisole)
    — fenbendazole-medicated feed is most common (effective against adults, larvae, and eggs)
    — consider side effects of tx (growth rate, electrolyt transport in GI tract, immune response to allergens, cardiac reactivity to beta-adrenergic stimulation, and interference with adjuvant arthritis
  • Decontaminate environment
  • Rederivation
218
Q

Diagnosis of Syphacia
muris

A

Maceration of cecum/colon with examination under stereomicroscope**
- most effective

ID of worms in large intestine (histopathology)

Touch tape

Fecal flotation, fecal concentration and centrifugation for eggs

PCR testing

219
Q

Pathogenesis of Aspiculuris tetraptera

A

Direct life cycles
- eggs are deposited in colon and passed in the feces
- eggs embryonate and become infectious
- new hosts become infected by ingestion of eggs in contaminated food or water or fomites

220
Q

Spp. susceptible to Syphacia
muris

A

Found in both mice and rats

221
Q

Histopath lesions of Syphacia
muris

A

Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases

222
Q

Treatment/control of Syphacia
muris

A
  • anthelmintic tx (fenbendazole, ivermectin, new generation avermectins, levamisole)
    — fenbendazole-medicated feed is most common (effective against adults, larvae, and eggs)
    — consider side effects of tx (growth rate, electrolyt transport in GI tract, immune response to allergens, cardiac reactivity to beta-adrenergic stimulation, and interference with adjuvant arthritis
  • Decontaminate environment
  • Rederivation
223
Q

Research impact of Syphacia
muris

A

Can vary from non to major significance

224
Q

Research impact of Syphacia
obvelata

A

Can vary from non to major significance

225
Q

Research impact of Aspiculuris tetraptera

A

Can vary from non to major signfiicance

226
Q

Treatment/control of Syphacia obvelata

A
  • anthelmintic tx (fenbendazole, ivermectin, new generation avermectins, levamisole)
    — fenbendazole-medicated feed is most common (effective against adults, larvae, and eggs)
    — consider side effects of tx (growth rate, electrolyt transport in GI tract, immune response to allergens, cardiac reactivity to beta-adrenergic stimulation, and interference with adjuvant arthritis
  • Decontaminate environment
  • Rederivation
227
Q

treatment/control of Aspiculuris tetraptera

A
  • anthelmintic tx (fenbendazole, ivermectin, new generation avermectins, levamisole)
    — fenbendazole-medicated feed is most common (effective against adults, larvae, and eggs)
    — consider side effects of tx (growth rate, electrolyt transport in GI tract, immune response to allergens, cardiac reactivity to beta-adrenergic stimulation, and interference with adjuvant arthritis
  • Decontaminate environment
  • Rederivation
228
Q

histopath lesions of Syphacia obvelata

A

Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases

229
Q

histopath lesions of Aspiculuris tetraptera

A

Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases

230
Q

Spp. susceptible to Syphacia
obvelata

A

More common in rats

231
Q

Spp. susceptible to Aspiculuris tetraptera

A

More common in mice

232
Q

Features of Trichosomoides crassicauda

A

(Bladder threadworm)

Adult females ~10mm long, males MUCH smaller

233
Q

pathogenesis of Trichosomoides crassicauda

A

Infects urinary tract of wild and lab rats

Females live in the lume and mucosa of renal pelvis and urinary bladder
— females burrow into the mucosa
—– males may reside in lumen or within the vagina/uterus of the female worms

Direct life cycle (8-9wks):
- double-operculated eggs passed in urine - > eggs ingested and hatch in stomach -> larvae penetrate stomach and migrate to various tissues (most die in these tissues) -> larvae that reach the urinary tract survive and develop into adults that mate and lay eggs

234
Q

histopath lesions of Trichosomoides crassicauda

A
  • migrating larvae can die in various tissues, resulting in small granulomas
  • Adult female worms are with the urinary bladder mucosa
  • mild uroepithelial hyperplasia of the bladder; mild pyelitis/pyelonephritis in the kidney
235
Q

treatment of Trichosomoides crassicauda

A

Ivermectin for tx

236
Q

Research impact of Trichosomoides crassicauda

A
  • hyperplastic lesions can be mistaken for neoplastic or preneoplastic lesions

Otherwise, no significant impact has been reported

237
Q

Features of Rodentolepis nana

A

(aka Hymenolepis nana)
Adults: 20-40mm long, 1mm wide

Four suckers on scolex and ARMED rostellum with hooks

238
Q

Is Rodentolepis nana zoonotic?

239
Q

Clinical signs of Rodentolepis nana

A

Rarely pathogenic in rats (may be severe in weanlings and young adults).
- decreased growth rate, weight loss, impaction, death

240
Q

diagnosis of Rodentolepis nana

A

Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation

241
Q

pathogenesis of Rodentolepis nana

A

Indirect OR direct lifecycle
- potential for autoinfection

242
Q

treatment of Rodentolepis nana

A
  • Generally, don’t treat due to zoonotic risk
  • insect control, wild rodent control
  • disinfection
  • purchase from trusted vendors
243
Q

Is Rodentolepis microstoma zoonotic?

244
Q

Clinical signs of Rodentolepis microstoma

A

Rarely pathogenic in rats (may be severe in weanlings and young adults)
- decreased growth rate, weight loss, impaction, death

245
Q

Diagnosis of Rodentolepis microstoma

A

Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation

246
Q

Treatment of Rodentolepis microstoma

A
  • Generally, don’t treat due to zoonotic risk
  • insect control, wild rodent control
  • disinfection
  • purchase from trusted vendors
247
Q

Features of Hymenolepis diminuta

A

Adults: 20-60mm long, 3-4mm wide

Four suckers on scolex and UNARMED rostellum

248
Q

Is Hymenolepis diminuta zoonotic

249
Q

Clinical signs of Hymenolepis diminuta

A

Rarely pathogenic in rats (may be severe in weanlings and young adults)
- decreased growth rate, weight loss, impaction, death

250
Q

Diagnosis of Hymenolepis diminuta

A

Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation

251
Q

pathogenesis of Hymenolepis diminuta

A

Indirect lifecycle with arthropod intermediate host

252
Q

treatment of Hymenolepis diminuta

A
  • Generally, don’t treat due to zoonotic risk
  • insect control, wild rodent control
  • disinfection
  • purchase from trusted vendors
253
Q

research impact of Hymenolepis diminuta

A

Shown to stimulate Th2 Type immune response, with systemic immune modulation

254
Q

Features of Taenia taeniaformis

A

“Cat tapeworm” (cats are definitive host, rats are intermediate hosts that become infected by cat feces)

Larval form within rats:
Cysticercus fasciolaris

255
Q

What is the larval form of Taenia taeniaformis in rats

A

Cysticercus fasciolaris

256
Q

Pathogenesis of Taenia taeniaformis

A

Eggs ingested by rat -> hatch and migrate to encyst within liver

Liver cysts associated with fibrosarcoma

257
Q

Features of Radfordia ensifera

A

(Fur mite)

Paired, equal-length claws on second leg (look like sloth claws)

258
Q

Transmission of Radfordia ensifera

A

Eggs persist in environment for long periods -> hatch in 7-8 days (females can lay eggs by day 16)

259
Q

Clinical signs of Radfordia ensifera

A

Usually none, unless heavy infestation, which leads to intense pruritis

260
Q

Diagnosis of Radfordia ensifera

A

***PCR of skin swab or cage swab very sensitive

Tape tests or skin scrapes
Mites on fur (migrate to tips of hair shafts postmortem)

261
Q

Pathogensis of Radfordia ensifera

A
  • live on the skin and fur of rats and mice, burrow into superficial dermis (usually dorsal neck and intrascapular region)
262
Q

Gross lesions of Radfordia ensifera

A

Hair loss and excoriation

263
Q

Treatment of Radfordia ensifera

A

Topical selamectin, moxidectin, ivermectin, and other tx

Clean the environment

264
Q

Research impacts of Radfordia ensifera

A

Effects on skin mitotic activity

Effects on immune modulation

265
Q

Notedres muris is the same as ____ but targets ___

A
  • Radfordia ensifera
  • ears
266
Q

What is polyplax spinulosa a vector for

A

Mycoplasma pulmonis

267
Q

What is polplax spinulosa

A

louse of rats

268
Q

What is the most common mammary tumor for rats > 2 years

A

Mammary fibroadenoma

269
Q

clinical signs of mammary fibroadenoma

A
  • Commonly located anywhere on the mammary chain
270
Q

Pathogenesis of mammary fibroadenoma

A

Occasionally found in males, predominantly females

Exposure to estrogen and prolonged exposure to prolactin increase tumor frequency (parity and ovariectomy decrease the incidence of mammary gland tumors)

271
Q

gross lesions of mammary fibroadenoma

A

Freely movable under SQ tissues, circumscribed, firm, lobulated

Large tumors may ulcerate

272
Q

Most common testicular cell tumor

A

Interstitial cell tumors (leydig cell tumors)

273
Q

clinical signs of testicular cell tumors

A

one or both testes
concurrent hypercalcemia

274
Q

Rats susceptible to testicular cell tumors

A

F-344 rats – 80% by 15 mos. Of age

275
Q

Gross lesions of testicular cell tumors

A
  • Single or multiple masses
  • light yellow to hemorrhagic
  • Circumscribed and lobulated
276
Q

Histopath lesions of testicular cell tumors

A

Sheets of cells of 2 types:
- polyhedral to elongated cells w/ vacuolated to granular cytoplasm
- Smaller cells w/ hyperchromatic nuclei and little cytoplasm

These cells extend between, compress, and often replace tubules

Hemorrhage, necrosis, mineralization, inflammation, cystic degeneration, tulular atrophy may occur

277
Q

Clinical signs of Pituitary gland adenoma

A

Vary from asymptomatic to head tilt, severe depression, ataxia

278
Q

pathogenesis of Pituitary gland adenoma

A

Originate from the Pars distalis of the pituitary gland

279
Q

Rats strains susceptible to Pituitary gland adenoma

A

Female F-344s and SDs and Wistar rats

Females > males
(mated females have reduced incidence compared to non-mated females)
- reducing caloric intake reduces incidence

280
Q

Gross lesions of Pituitary gland adenoma

A

Vary in size, but may be up to 0.5cm in diameter
Soft and dark red due to prominent hemorrhage
Well-circumscribed and often compress adjacent brain tissue -> hydrocephalus

281
Q

Pathogenesis of Zymbal’s gland tumor

A

Arise from holocrine glands in the subcutis at the base of the external ear
(“arises from the squamous lining of the deeper aspect of the ear canal. Well demarcated, non-invasive, multilobulated, and nonencapsulated neoplasm

282
Q

Gross lesions of Zymbal’s gland tumor

A

Consists of papillary projections of stratified squamous epithelium supported by expanded fibrovascular cores. The basement membrane is intact.

283
Q

Pancreatic islet cell tumor strains susceptibility

A

Wistar Han > F-344

Male SD > female SD

Pheochromocytomas more prominent in male F-344s than females

284
Q

Clinical signs of Large granular lymphocytic leukemia

A
  • anemia
  • Concurrent IMHA
  • Jaundice
  • Weight loss
  • Splenomegaly +/- hepatomegaly
  • Leukocytosis (up to 400,000/mL)(
  • Infiltration of malignant lymphocytes in various organs
285
Q

Gross lesions of pancreatic islet tumors

A

Single or multiple and are circumscribed and reddish brown.

Islet cell carcinomas are distinguished from adenomas by capsular invasion and metastases.

Tumors of the exocrine pancreas are less common

Adrenal tumors are relatively common endocrine tumors in rats. Can affect medulla and cortex (may be difficult to differentiate from hyperplasia)

286
Q

pathogenesis of Large granular lymphocytic leukemia

A

Originates in spleen, lymphocytic in origin; not associated w/ a retrovirus like mice

287
Q

rat strain susceptibility of Large granular lymphocytic leukemia

A

Observed in up to 50% of F-344s

Wistar and Wistar-Furth rats also affected

288
Q

Histopath lesions of Large granular lymphocytic leukemia

A
  • Prominent azurophilic cytoplasmic granules
289
Q

Rat strain susceptibility of histiocytic sarcoma

A

SDs
Wistar
Osborne-Mendel rats

290
Q

gross lesions of histiocytic sarcoma

A

Present in lung, liver, LN, SQ, mediastinum, retroperitoneum

Grossly pale, firm and displace normal tissue

291
Q

T/F Hydronephrosis is often an incidental finding during necropsy

292
Q

Rat strain susceptibility of hydronephrosis

A

Inheritied as a single dominant gene in Gunn Rats

Polygenic in Brown Norway and SD rats

293
Q

gross lesions of hydronephrosis

A

Lesions vary in severity and structures affected
- Kidney consists of a fluid-filled sac
- Dilated pelvis contains clear serous fluid

294
Q

histopath lesions of hydronephrosis

A
  • Marked dilation of the renal pelvis
  • no inflammatory response
  • shortened renal tubules
295
Q

ddx of hydronephrosis

A

Pyelonephritis, polycystic kidneys, renal papillary necrosis

296
Q

What is one of the most common causes of death in aged rats

A

Chronic progressive nephropathy

297
Q

Clinical signs of Chronic progressive nephropathy

A
  • proteinuria
  • weight loss
    Increased plasma creatinine

In late stages: hypertension and polyarteritis nodosa

298
Q

pathogenesis of Chronic progressive nephropathy

A

Overfeeding -> prolonged increase in renal blood flow and GFR -> hyperfiltration -> glomerular hypertrophy -> macromolecule filtration deficits, mesangial damage, glomerulosclerosis, protein leakage -> weight loss, proteinuria, azotemia -> death

299
Q

rat strain susceptibility to Chronic progressive nephropathy

A

F-344 and SD&raquo_space; Wistar and Long-Evans

Rats > 12 mos. More susceptible

Male&raquo_space; female

Unrestricted diet
High protein diets

300
Q

gross lesions of Chronic progressive nephropathy

A

Pitted and irregular renal cortices

Linear streaks may be present on cortex and medulla on cut surfaces

Brown pigmentation may be present

301
Q

What is nephrocalcinosis

A
  • deposition of calcium phosphate in renal tissues
302
Q

Diagnosis of Nephrocalcinosis

A

Von Kossa staining to ID presence of mineral (calcium) at corticomedullary junction

303
Q

Pathogenesis of Nephrocalcinosis

A

Predisposing factors: calcium, phosphorus, and magnesium imbalances

304
Q

Rat strain susceptibility of Nephrocalcinosis

A

Females more likely to develop dz

F-344(50%) and BDIX rats more likely to be affected

BDIX is model, incidence esp. high in BDIX rats (agouti color, used for teratogenesis and carcinogenesis studies)

Lowered incidence in SD and Wistar

305
Q

pathogenesis of Polyarteritis nodosa

A

Chronic, progress degenerative dz that most often occurs in the muscular medium-sized arteries of the mesentery, pancrease, pancreaticoduodenal artery, and testis, (and more) but spares the pulmonary circulation, large arteries, and glomeruli

Most commonly affected myocardial sites are papillary muscles and interventricular septum

306
Q

rat strain susceptibility of Polyarteritis nodosa

A

Commonly identified in male aged rats

Most often in SD and spontaneously hypertensive (SHR) strains

307
Q

gross lesions of Polyarteritis nodosa

A

Thick, tortuous gray to red, hard, medium-zied muscular arteries

***spares pulmonary arteries, large arteries, and glomeruli

Focal hemorrhage
May have aneurysmal dilatations

308
Q

histopath lesions of Polyarteritis nodosa

A

Fibrinoid necrosis w/ neutropilic and mononuclear infiltration of the intima and media

309
Q

Which rats are most susceptible to urolithiasis

A

Zucker diabetic fatty rats

310
Q

What predisposes a rat to ringtail

A

Keratin defect
- low humidity (<25%)
- genetics
- low environmental temperature
- dehydration
- poor nutrition

311
Q

histopath lesions of ringtail

A

Epidermal hyperplasia w/ orthokeratotic and parakeratotic hyperkeratosis

Dilated and thrombosed vessels observed in severe cases, accompanied by necrosis, hemorrhage, and coagulative necrosis of the overlying epidermis.

312
Q

treatment of ringtail

A

Topical application of lanolin was found to be beneficial in the tx of this dz

313
Q

Effects of hypovitaminosis A

314
Q

Effect of Hypovitaminosis E

A

testicular degeration

315
Q

Effect of hypovitaminosis K

A

Widespread hemorrhage due to loss of vitamin K-dependent coagulation factors (II, VII, IX, and X plus proteins C, S, and Z)

Path review (9 decks)

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