Rat Pathology Review Flashcards
(315 cards)
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)
2
Q
Which rat parvovirus is the only strain to produce natural disease?
A
Rat virus (RV; Kilham’s rat virus
3
Q
Features of Rat virus
A
Parvovirus, ssDNA
4
Q
Rat Virus causes what clinical signs/issues in pregnant females?
A
- infertility
- fetal resorption
- abortion
5
Q
T/F Pups infected w/ Rat virus in-utero will clear the infection
A
False, they will be persistently infected
6
Q
Where can Rat Virus be found in persistently infected rats?
A
Lymphoid tissues, endothelium, vascular muscle, and renal tubule epithelium
7
Q
Diagnosis of Rat Virus
A
- Serology
- PCR for DNA in tissue, feces, or environment
8
Q
Rat Virus Pathogenesis
A
- Infects cells in S-Phase (dna synthesis) of cell cycle
- Attacks endothelial cells and megakaryocytes (think hemorrhage)
9
Q
Which phase does Rat Virus infect cells?
A
S-Phase (DNA synthesis)
10
Q
How does Rat Virus cause damage?
A
Attacks endothelial cells and megakaryocytes
11
Q
Which rats spp. are susceptible to Rat Virus
A
- Athymic nude rats are more susceptible
- Immunocompetent rats can prevent clinical infection
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
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
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
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
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
17
Q
Features of Sendai Virus
A
Respirovirus of paramyxoviridae family (-ssDNA)
18
Q
Transmission of Sendai Virus
A
???
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
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)
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
22
Q
Susceptible rat strains to Sendai Virus
A
Brown Norway and LEW rats
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
24
Q
Research Impact of Sendai Virus
A
- Any respiratory research might be affected
- May impact immune responses to research target
25
Features of Sialodacryoadenitis virus (RCV-ADA)
- Coronavirus
- +ssRNA (tends to mutate more frequently than DNA)
26
Transmission of Sialodacryoadenitis virus
- Direct contact (nasal secretions, saliva)
- Aerosols
- Fomites
27
Do different coronaviruses provide protection against others?
No. Reinfection by same strain also possible, but CS less severe
28
Clinical signs of Sialodacryoadenitis virus
- **** 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)
29
Morbidity / mortality of Sialodacryoadenitis virus
high morbidity / low mortality
30
Diagnosis of Sialodacryoadenitis virus
- MFIA serology
- PCR from affected glands
- Histopath can be helpful in CLINICAL cases
31
Which strains are susceptible to Sialodacryoadenitis virus?
- 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)
32
Gross lesions of Sialodacryoadenitis virus
- ****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
33
Histopath lesions of Sialodacryoadenitis virus
- 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
34
Describe the Two stages of Sialoacryoadenitis virus
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
35
Prevention of Sialodacryoadenitis virus
Prevention:
- know pathogen status of vendor
- Effective quarantine programs
- keep separate from wild rats
36
Control of Sialoacryoadenitis virus
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
37
Research Impacts of Sialodacryoadenitis virus
- 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)
38
Features of Polyomavirus
- small dsDNA polyomavirus
39
Clinical signs of rat polyomavirus
- ***wasting, nonsuppurative sialoadenitis, dyspnea, and interstitial pneumonia
40
Rat Strains susceptible to Rat Polyomavirus
- Athymic nude rats susceptible
- Euthymic rats NOT susceptible
41
Histopathological lesions of rat Polyomavirus
- 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”)
42
Features of Rotavirus
Group B rotavirus, dsRNA, possibly of human origin
43
Transmission of Rat Rotavirus
-Fecal oral (feces and fomites)
44
Clinical signs of Rat Rotavirus
-**** diarrhea within 24-36 hours
- slowed growth
45
Gross lesions of rat rotavirus
- 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
46
Histopath lesions of rat rotavirus
- ****Pathognomonic epithelial syncytia w/ variably present eosinophilic intracytoplasmic inclusions
- Intestinal villus attenuation, necrosis of enterocytes
47
What is the biggest concern for Cowpox virus
The zoonotic potential
48
Features of Cowpox virus
- orthopoxvirus, dsDNA
49
Clinical signs of cowpox virus
CS may vary:
- may be subclinical
-proliferating and necrotizing circular dermal lesions
- Acute pulmonary form w/ high mortality (intranasal inoculation leads to peracute mortality)
50
Morbidity/mortality of cowpox virus
Enzootic among rodents;
(humans, cattle, felids, and some other mammals susceptible)
High mortality w/ acute pulmonary form
51
Gross lesions of cowpox virus
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
52
Histopath lesions of cowpox virus
- Hyperplasia and necrosis of epithelium
- bronchointerstitial pneumonia, congestion, eema
- large eosinophilic intracytoplasmic inclusion bodies (Guarnieri bodies)
- Lymphoid necrosis
53
Features of Rat Cytomegalovirus
- Beta-herpesvirus
54
Clinical signs of rat cytomegalovirus
often subclinical
55
Pathogenesis of rat cytomegalovirus
- Infects salivary and lacrimal glands
- Cytomegaly w/ intracytoplasmic and intranuclear inclusions in ductal epithelium
- nonsuppurative interstitial inflammation
56
Rat strains susceptible to Rat Cytomegalovirus
not really seen in lab rats, common in wild rats
57
Features of Rat Theilovirus
Cardiovirus genus
58
transmission of Theilovirus
Fecal-oral
59
Clinical signs of Theilovirus
Often subclinical
60
Diagnosis of rat Theilovirus
Serology
61
Pathogenesis of Rat Theilovirus
¬Replicates in small intestinal enterocytes; shed in feces for 4-8 weeks
62
Rat Strains susceptible to Rat Theilovirus
Nude rats: infection leads to Persistent shedding, virus found in intestines and elsewhere
63
Gross and histopath changes of Rat Theilovirus
No gross or histopath changes
64
Control/prevention of Rat Theilovirus
Control via test and cull
65
Features of Pneumonia Virus of Mice (PVM)
- Pneumovirus of paramyxoviridae family
66
Clinical signs of Pneumonia Virus of Mice
subclinical infection
67
Pathogenesis/concerns of Pneumonia Virus of Mice
** possibly a significant co-pathogen w/ Mycoplasma pulmonis
68
What species does pneumonia virus of mice infect?
Infects mice, rats, hamsters, gerbils, guinea pigs, and rabbits
69
Histopath lesions of Pneumonia Virus of Mice
Vasculitis, interstitial pneumonitis w/ necrosis
70
Primary concern of Hantavirus
ZOONOTIC
71
What are the human diseases associated with hantavirus
(Seoul Hantavirus causes hemorrhagic fever w/ renal syndrome in humans); (hantavirus pulmonary syndrome in Florida)
72
Features of hantavirus
Bunyaviridae family
73
Clinical signs of Hantavirus
Chronic, subclinical infection
74
T/F Rodents are not natural reservoirs for Hantavirus
False, they are
75
Transmission of Hantavirus of Rats
virus shed in feces and urine
76
Does Rat Adenovirus cause clinical disease
no
77
Histopath lesions associated with Rat Adenovirus
Inclusions can be seen in enterocytes, typically incidental findings
78
Features of Filobacterium Rodentium
(formerly Cilia-Associated Respiratory (CAR) Bacillus)
- filamentous, G- argyophilic
79
Transmission of Filobacterium Rodentium
- direct (oronasal) contact, usually in young (neonatal) rats
80
Severity and Clinical signs of Filobacterium Rodentium
Severity variable
(may be clinical, subclin., or only clinical if copathogen present)
CS:
- Oculonasal discharge, increased resp. effort, hunched posture, anorexia w/ weight loss
81
Diagnosis of Filobacterium Rodentium
- PCR from nasopharyngeal or tracheal swabs
- Serology (ELISA, MFIA, IFA)
- ID of org. w/ silver stains (like Warthin-Starry staining)
82
Pathogenesis of Filobacterium rodentium
- 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
83
Which rat strains are susceptible to Filobacterium rodentium
all strains
84
Gross lesions of Filobacterium Rodentium
- 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
85
Histopath lesions of Filobacterium rodentium
- 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
86
Control of Filobacterium rodentium
Control:
- evaluate risk of wild rodent exposure
- Test and cull and/or depop-repop
87
Research impact of Filobacterium rodentium
- 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
88
Features of Mycoplasma pulmonis
- (G-); very small
- Lacks a cell wall entirely
89
transmission of Mycoplasma pulmonis
- direct contact
- Aerosolization
- Transplacental
90
Which is more likely to present clinical signs: Filobacterium rodentium or Mycoplasma pulmonis
Mycoplasma pulmonis
91
Clinical signs of Mycoplasma pulmonis
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)
92
Diagnosis of Mycoplasma pulmonis
- 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.
93
Pathogenesis of Mycoplasma pulmonis
**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
94
Susceptible strains of Mycoplasma pulmonis
All strains
95
Gross lesions of Mycoplasma pulmonis
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
96
Histopath lesions of Mycoplasma pulmonis
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
97
Control of Mycoplasma pulmonis
Control:
- reputable vendors
- quarantine and screening
Prevent exposure to wild rodents
- Depop and repop
98
Research Impact of Mycoplasma Pulmonis
- Impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
99
What is the Etiology of Chronic Respiratory Disease of Rats
Etiology:
- Mycoplasma pulmonis (the major causative agent)
- CAR Bacillus (Filobacterium rodentium)
- Sendai virus
- Rat Coronavirus (Sialodenacryoadentitis virus)
- Ammonia exposure above 25ppm
100
Features of Corynebacterium kutscheri
- (G+); short rod
101
Transmission of Corynebacterium kutscheri
- Predominantly fecal-oral
- Direct contact
102
Clinical signs of Corynebacterium kutscheri
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
103
Diagnosis of Corynebacterium kutscheri
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)
104
Pathogenesis of Corynebacterium kutscheri
Carried in oropharynx and Regional LNs for weeks -> hematogenous spread to many organs
105
Strains / spp. susceptible to Corynebacterium kutscheri
Can infect mice, rats, and guinea pigs
Any age can be affected
Immunocompromised rats most at risk of infection
106
Gross lesions of Corynebacterium kutscheri
- Red crusty lesions around eyes and nares
- possibly mucopurulent exudate around nose
- raised pale tan to white foci on lungs and possibly other organs
107
What is the causative agent of pseduotuberculosis
Corynebacterium kutscheri
108
Histo lesions of corynebacterium kutscheri
- 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)
109
control of corynebacterium kutscheri
Control:
- depop. And repop
- Sterilization
110
Research impact of corynebacterium kutscheri
- impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
111
Features of Clostridium piliforme
- (G-); filamentous rod
(other clostridium spp. Are often G+)
112
Transmission of Clostridium piliforme
Forms spores (can survive in the environment for up to 1 year)
- ingestion of spores from the environment
- fecal oral
113
Morbidity / mortality of Clostridium piliforme
(Tyzzer’s disease)
Low morb. / Hight mort.
(often acute death w/o any clinical signs)
114
Diagnosis of Clostridium piliforme
- (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)
115
Rats strains susceptible to Clostridium piliforme
Affects many animal spp.
- spp.-specific variations in lesions
- Young rats in the postweaning period more susceptible to dz
116
gross lesions of Clostridium piliforme
- Small white foci throughout the liver and heart
- ***Megaloileitis: flaccid and dilated ileum filled w/ hemorrhage
117
Histo lesions of Clostridium piliforme
- 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
118
pathognomonic lesions of Clostridium piliforme
- Megaloileitis: flaccid and dilated ileum filled w/ hemorrhage
119
Control and prev. of Clostridium piliforme
Control and prev.
- keep facilities clean
- prevent exposure to wild animals (wide range of hosts and persistence of spores)
120
Research impact of Clostridium piliforme
- Clinically sick animals
- sudden death of animals, esp. young animals
121
Research impact of Streptococcus pneumoniae
- Impact on animal health and number of possibly affected organ systems means that infected animals are unfit for research
122
Control of Streptococcus pneumoniae
Control:
- Reputable vendors
- Quarantine and screening
- Depop if indicated
123
Histo lesions of Streptococcus pneumoniae
- Fibrinopurulent (fibrin, degenerate neutrophils), polyserositis, and bronchopneumonia
- embolic neutrophilic inflammation in liver and other organs
124
Gross lesions of Streptococcus pneumoniae
-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
125
Rat strains/ages susceptible to Streptococcus pneumoniae
Young rats may develop disease
126
Diagnosis of Streptococcus pneumoniae
- Nasopharyngeal culture via blood agar place, optochin inhibition test
- PCR
Tests are best w/ histopath to corroborate, since there are nonpathogenic strains
127
Clinical signs of Streptococcus pneumoniae
Often subclinical
- Dyspnea
- serous to mucopurulent nasal discharge
128
Transmission of Streptococcus pneumoniae
- Aerosol
- Fomites
ZOONOTIC
(humans are the natural host for this bacteria -> potential reverse zoonosis)
129
Features of Streptococcus pneumoniae
- (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
Features of Bordetella bronchiseptica
- (G-), coccobaccili
131
Clinical signs of Bordetella bronchiseptica
- Suppurative rhinitis w/ multifocal bronchopneumonia and peribronchial lymphoid hyperplasia (cranioventral pneumonia)
132
diagnosis of Bordetella bronchiseptica
Must be able to isolate the bacteria in large #s for definitive dx, and look for copathogens
133
Morbidity / mortality of Enterococcus
Epizootics of enteric dz in suckling rats w/ high morbity and high mortality
134
Features of Enterococcus
(entercoccal enteropathy)
- (G+) cocci
- part of normal rat microbiome
135
Clinical signs of Enterococcus
- diarrhea, fecal staining of fur
- stunted growth, distended abdomens
136
Diagnosis of Enterococcus
Combo of CS w /ID of bacteria on histology
137
histo lesions of enterococcus
- Large #s of G+ coccoid bacteria lining otherwise normal enterocytes in the sm. intestine
138
gross lesions of enterococcus
- stomachs distended w/ milk (still have good appetite)
- Dilation of small and large intestines w/ gas and fluid
139
research impact of Helicobacter
Nothing significant as long as the animals are not clinical
140
Control of Helicobacter
Control:
- Treat individuals or small groups w/ abx (amoxicillin, clarithromycin, metronidazole, omeprazole)
141
histo lesions of Helicobacter
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
Gross lesions of Helicobacter
In athymic nude mice:
- Proliferative and ulcerative typhlitis, colitis, and proctitis
(The wall itself is thickened, not just enlarged)
143
rat strains susceptible to Helicobacter
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
diagnosis of Helicobacter
- 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
transmission of Helicobacter
feces most likely
146
features of Helicobacter
- (G-); flagellated; spiral, curved, or straight
Many spp. ID’ed in lab animals, including several in rats
147
Features of Lawsonia intracellularis
- (G-) argryophlic, small, curved rod
Obligate intracellular org. that lives inside the cytoplasm of infected host’s enterocytes
148
Susceptible rat strains to Lawsonia intracellularis
Significant dz in hamsters and rabbits, less so in rats
149
gross lesions of Lawsonia intracellularis
Proliferative enteritis
150
histo lesions of Lawsonia intracellularis
- 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
Is Clostridium difficile a significant cause of dz in rats?
No, but it can cause enterotoxemia in rats under certain conditions due to toxin formation
152
Features of Salmonella enterica
(G-) w/ wide host range
2,500+ serovars in S. enterica spp
Rare in lab animals but common in wild animals
153
Clinical signs of Salmonella enterica
Often subclinical (think Typhoid Mary)
- nonspecific signs (lethargy, wt. loss)
- soft stools and diarrhea
- acute death
154
Diagnosis of Salmonella enterica
PCR or Culture
- Mesenteric lymph nodes
- Repeated fecal samplings (salmonella may be intermittently present, esp. in carriers
155
Pathogenesis of Salmonella enterica
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
Gross lesions of Salmonella enterica
- Thickened and ulcerated intestines (cecum and ileum)
- Splenomegaly
- Multiple small, white-yellow spots on liver
- enlarged LNs
157
Histo lesions of Salmonella enterica
- 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
Control/prev. of Salmonella enterica
- Reputable vendors
- Quarantine and screening
- Good hygiene (animals and humans)
- Prevent exposure to wild rodents
- Depop and deep cleaning if positive
159
Research impact of Salmonella enterica
Zoonotic risk, do not use any animals from an infected population
160
T/F Campylobacter jejuni is not zoonotic
false, it is
161
Clinical signs of campylobacter jejuni
Usually subclinical
Mild diarrhea in young rats possible
162
Susceptible strains of Campylobacter jejuni
Wide range of possible hosts (gastroenteritis in humans)
163
histo lesions of Staphylococcus aureus
- 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
Gross lesions of Staphylococcus aureus
- 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
Rat strains susceptible to Staphylococcus aureus
--- NK-cell-deficient beige rats are most susceptible, esp. males, w/ dz similar to Chediak-Higashi syndrome
166
Pathogenesis of Staphylococcus aureus
- 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
diagnosis of Staphylococcus aureus
Ulcerative skin lesions w/ G+ cocci are diagnostic
Culture of coagulase-positive S. aureus
168
clinical signs of Staphylococcus aureus
usually subclinical
169
features of Staphylococcus aureus
- (G+) cocci
Ubiquitous commensal bacteria of skin and mucous membranes
170
features of Streptobacillus moniliformis
- (G-) pleomorphic rod to filamentous bacteria
Commensal org. in nasopharynx of rats (also in blood and urine in cases of infection)
171
What is the major concern of Streptobacillus moniliformis
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
Transmission of Streptobacillus moniliformis
Transmission can occur through bites, close contact w/ infected rats, or inadvertent ingestion of rat feces/urine
173
transmission of Pasteurella pneumotropica
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
clinical signs of pasteurella pneumotropica
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
Research impact of pasteurella pnemotropica
- No impact unless animals are clinically ill
- No effort required to remove from colony unless immunodeficient animals are present
176
transmission of Pseudomonas
aeruginosa
- 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
clinical signs of Pseudomonas
aeruginosa
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
diagnosis of Pseudomonas
aeruginosa
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
research impact of Pseudomonas
aeruginosa
Depends on studies using these techniques
180
Transmission of Mycoplasma muris
- transmitted primarily by Polyplax spinulosa
181
clinical signs of Mycoplasma muris
- 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
Is Klebsiella pneumoniae zoonotic
yes
183
clinical signs of Klebsieall pneumoniae
Minimal inflammation, typically a nonpurulent interstitial nephritis
Rats important as carriers
184
Causes of hepatic necrosis in rats
- Bacterial: Clostridium piliforme, Corynebacterium kutscheri)
- Viral: rat virus (parvovirus)
185
Transmission of Pneumocystis
carinii
- Aerosol
- possibly fomites
186
clinical signs of Pneumocystis
carinii
Dyspnea
Cyanosis
Weight loss
187
diagnosis of Pneumocystis
carinii
Special stains
PCR of lung tissue, bronchiolar lavage, or oral swabs
Serology 6-8 wks after infection
188
Pathogenesis of Pneumocystis
carinii
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
Gross lesions of Pneumocystis
carinii
- lungs fail to collapse
- fel small pale tan or white foci on lung surface
190
Histo lesions of Pneumocystis
carinii
- interstitial pneumonia with neutrophils and histiocytes
- Very high numbers of intra-alveolar histiocytes
- lymphocytes around airways
191
Research impact of Pneumocystis
carinii
Unknown w/ immunocompetent rats
Possible impact for inhalation/anesthesia studies
192
Features of Trichophyton mentagrophytes
(Dermatophytosis, aka Ringworm)
- most common dermatophyte of rats, mice, rabbits
193
Transmission of Trichophyton mentagrophytes
More common in wild and pet rats
Direct contact, fomites
ZOONOTIC
194
diagnosis of Trichophyton mentagrophytes
Special stains w/ fungi on hair shafts
Fungal culture
Skin-scrapings
195
gross lesions of Trichophyton mentagrophytes
- patchy hair loss
- erythematous to pustular lesions
196
Histopath lesions of Trichophyton mentagrophytes
Hyperkeratosis, epidermal hyperplasia, leukocytic dermatitis and folliculitis
197
clinical signs of Aspergillus
Chronic rhinitis w/ fungal hyphae
198
research impact of aspergillus
Potential for lung involvement
199
Gross lesions of Blastomyces
dermatiditis
- Gray-white lung nodules
- Bronchopneumonia w/ pyogranulomas
- thick-walled yeast forms
200
Which spp. does encephalitozoon cuniculi affect typically
primarily a disease of rabbits
201
Features of Cryptosporidium
- intracellular parasite of intestinal epithelial cells (present within the cell but not the cytoplasm)
202
Clinical signs of Cryptosporidium
Transient and mild disease in immunocompetent animals
203
Rat strains susceptible to Cryptosporidium
Immunosuppressed or athymic rats may be susceptible to clinical disease
Outbreak of diarrhea and high mortality among infant rats in Rapp hypertensive strain
204
Features of Syphacia muris
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
Features of Syphacia obvelata
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
Features of Aspiculuris tetraptera
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
Transmission of Syphacia
muris
Fecal-oral
Fomites
Contaminated water
208
Transmission of Syphacia
obvelata
Fecal-oral
Fomites
Contaminated water
209
Transmission of Aspiculuris tetraptera
Fecal-oral
Fomites
Contaminated water
210
Clinical signs of Syphacia
muris
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
Clinical signs of Syphacia
obvelata
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
Clinical signs of Aspiculuris tetraptera
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
Diagnosis of Syphacia
muris
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
Pathogenesis of Syphacia
muris
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
Pathogenesis of Syphacia
obvelata
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
Diagnosis of Aspiculuris tetraptera
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
Treatment/control of Syphacia
obvelata
- 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
Diagnosis of Syphacia
muris
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
Pathogenesis of Aspiculuris tetraptera
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
Spp. susceptible to Syphacia
muris
Found in both mice and rats
221
Histopath lesions of Syphacia
muris
Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases
222
Treatment/control of Syphacia
muris
- 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
Research impact of Syphacia
muris
Can vary from non to major significance
224
Research impact of Syphacia
obvelata
Can vary from non to major significance
225
Research impact of Aspiculuris tetraptera
Can vary from non to major signfiicance
226
Treatment/control of Syphacia obvelata
- 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
treatment/control of Aspiculuris tetraptera
- 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
histopath lesions of Syphacia obvelata
Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases
229
histopath lesions of Aspiculuris tetraptera
Adults are present in GI tract (prominent lateral alae)
- granulomatous inflammation in some cases
230
Spp. susceptible to Syphacia
obvelata
More common in rats
231
Spp. susceptible to Aspiculuris tetraptera
More common in mice
232
Features of Trichosomoides crassicauda
(Bladder threadworm)
Adult females ~10mm long, males MUCH smaller
233
pathogenesis of Trichosomoides crassicauda
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
histopath lesions of Trichosomoides crassicauda
- 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
treatment of Trichosomoides crassicauda
Ivermectin for tx
236
Research impact of Trichosomoides crassicauda
- hyperplastic lesions can be mistaken for neoplastic or preneoplastic lesions
Otherwise, no significant impact has been reported
237
Features of Rodentolepis nana
(aka Hymenolepis nana)
Adults: 20-40mm long, 1mm wide
Four suckers on scolex and ARMED rostellum with hooks
238
Is Rodentolepis nana zoonotic?
yes
239
Clinical signs of Rodentolepis nana
Rarely pathogenic in rats (may be severe in weanlings and young adults).
- decreased growth rate, weight loss, impaction, death
240
diagnosis of Rodentolepis nana
Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation
241
pathogenesis of Rodentolepis nana
Indirect OR direct lifecycle
- potential for autoinfection
242
treatment of Rodentolepis nana
- Generally, don’t treat due to zoonotic risk
- insect control, wild rodent control
- disinfection
- purchase from trusted vendors
243
Is Rodentolepis microstoma zoonotic?
yes
244
Clinical signs of Rodentolepis microstoma
Rarely pathogenic in rats (may be severe in weanlings and young adults)
- decreased growth rate, weight loss, impaction, death
245
Diagnosis of Rodentolepis microstoma
Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation
246
Treatment of Rodentolepis microstoma
- Generally, don’t treat due to zoonotic risk
- insect control, wild rodent control
- disinfection
- purchase from trusted vendors
247
Features of Hymenolepis diminuta
Adults: 20-60mm long, 3-4mm wide
Four suckers on scolex and UNARMED rostellum
248
Is Hymenolepis diminuta zoonotic
yes
249
Clinical signs of Hymenolepis diminuta
Rarely pathogenic in rats (may be severe in weanlings and young adults)
- decreased growth rate, weight loss, impaction, death
250
Diagnosis of Hymenolepis diminuta
Direct examination of adults, grossly histopathologic ID, or fecal smear/flotation
251
pathogenesis of Hymenolepis diminuta
Indirect lifecycle with arthropod intermediate host
252
treatment of Hymenolepis diminuta
- Generally, don’t treat due to zoonotic risk
- insect control, wild rodent control
- disinfection
- purchase from trusted vendors
253
research impact of Hymenolepis diminuta
Shown to stimulate Th2 Type immune response, with systemic immune modulation
254
Features of Taenia taeniaformis
“Cat tapeworm” (cats are definitive host, rats are intermediate hosts that become infected by cat feces)
Larval form within rats:
Cysticercus fasciolaris
255
What is the larval form of Taenia taeniaformis in rats
Cysticercus fasciolaris
256
Pathogenesis of Taenia taeniaformis
Eggs ingested by rat -> hatch and migrate to encyst within liver
Liver cysts associated with fibrosarcoma
257
Features of Radfordia ensifera
(Fur mite)
Paired, equal-length claws on second leg (look like sloth claws)
258
Transmission of Radfordia ensifera
Eggs persist in environment for long periods -> hatch in 7-8 days (females can lay eggs by day 16)
259
Clinical signs of Radfordia ensifera
Usually none, unless heavy infestation, which leads to intense pruritis
260
Diagnosis of Radfordia ensifera
***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
Pathogensis of Radfordia ensifera
- live on the skin and fur of rats and mice, burrow into superficial dermis (usually dorsal neck and intrascapular region)
262
Gross lesions of Radfordia ensifera
Hair loss and excoriation
263
Treatment of Radfordia ensifera
Topical selamectin, moxidectin, ivermectin, and other tx
Clean the environment
264
Research impacts of Radfordia ensifera
Effects on skin mitotic activity
Effects on immune modulation
265
Notedres muris is the same as ____ but targets ___
- Radfordia ensifera
- ears
266
What is polyplax spinulosa a vector for
Mycoplasma pulmonis
267
What is polplax spinulosa
louse of rats
268
What is the most common mammary tumor for rats > 2 years
Mammary fibroadenoma
269
clinical signs of mammary fibroadenoma
- Commonly located anywhere on the mammary chain
270
Pathogenesis of mammary fibroadenoma
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
gross lesions of mammary fibroadenoma
Freely movable under SQ tissues, circumscribed, firm, lobulated
Large tumors may ulcerate
272
Most common testicular cell tumor
Interstitial cell tumors (leydig cell tumors)
273
clinical signs of testicular cell tumors
one or both testes
concurrent hypercalcemia
274
Rats susceptible to testicular cell tumors
F-344 rats – 80% by 15 mos. Of age
275
Gross lesions of testicular cell tumors
- Single or multiple masses
- light yellow to hemorrhagic
- Circumscribed and lobulated
276
Histopath lesions of testicular cell tumors
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
Clinical signs of Pituitary gland adenoma
Vary from asymptomatic to head tilt, severe depression, ataxia
278
pathogenesis of Pituitary gland adenoma
Originate from the Pars distalis of the pituitary gland
279
Rats strains susceptible to Pituitary gland adenoma
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
Gross lesions of Pituitary gland adenoma
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
Pathogenesis of Zymbal's gland tumor
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
Gross lesions of Zymbal's gland tumor
Consists of papillary projections of stratified squamous epithelium supported by expanded fibrovascular cores. The basement membrane is intact.
283
Pancreatic islet cell tumor strains susceptibility
Wistar Han > F-344
Male SD > female SD
Pheochromocytomas more prominent in male F-344s than females
284
Clinical signs of Large granular lymphocytic leukemia
- anemia
- Concurrent IMHA
- Jaundice
- Weight loss
- Splenomegaly +/- hepatomegaly
- Leukocytosis (up to 400,000/mL)(
- Infiltration of malignant lymphocytes in various organs
285
Gross lesions of pancreatic islet tumors
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
pathogenesis of Large granular lymphocytic leukemia
Originates in spleen, lymphocytic in origin; not associated w/ a retrovirus like mice
287
rat strain susceptibility of Large granular lymphocytic leukemia
Observed in up to 50% of F-344s
Wistar and Wistar-Furth rats also affected
288
Histopath lesions of Large granular lymphocytic leukemia
- Prominent azurophilic cytoplasmic granules
289
Rat strain susceptibility of histiocytic sarcoma
SDs
Wistar
Osborne-Mendel rats
290
gross lesions of histiocytic sarcoma
Present in lung, liver, LN, SQ, mediastinum, retroperitoneum
Grossly pale, firm and displace normal tissue
291
T/F Hydronephrosis is often an incidental finding during necropsy
True
292
Rat strain susceptibility of hydronephrosis
Inheritied as a single dominant gene in Gunn Rats
Polygenic in Brown Norway and SD rats
293
gross lesions of hydronephrosis
Lesions vary in severity and structures affected
- Kidney consists of a fluid-filled sac
- Dilated pelvis contains clear serous fluid
294
histopath lesions of hydronephrosis
- Marked dilation of the renal pelvis
- no inflammatory response
- shortened renal tubules
295
ddx of hydronephrosis
Pyelonephritis, polycystic kidneys, renal papillary necrosis
296
What is one of the most common causes of death in aged rats
Chronic progressive nephropathy
297
Clinical signs of Chronic progressive nephropathy
- proteinuria
- weight loss
Increased plasma creatinine
In late stages: hypertension and polyarteritis nodosa
298
pathogenesis of Chronic progressive nephropathy
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
rat strain susceptibility to Chronic progressive nephropathy
F-344 and SD >> Wistar and Long-Evans
Rats > 12 mos. More susceptible
Male >> female
Unrestricted diet
High protein diets
300
gross lesions of Chronic progressive nephropathy
Pitted and irregular renal cortices
Linear streaks may be present on cortex and medulla on cut surfaces
Brown pigmentation may be present
301
What is nephrocalcinosis
- deposition of calcium phosphate in renal tissues
302
Diagnosis of Nephrocalcinosis
Von Kossa staining to ID presence of mineral (calcium) at corticomedullary junction
303
Pathogenesis of Nephrocalcinosis
Predisposing factors: calcium, phosphorus, and magnesium imbalances
304
Rat strain susceptibility of Nephrocalcinosis
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
pathogenesis of Polyarteritis nodosa
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
rat strain susceptibility of Polyarteritis nodosa
Commonly identified in male aged rats
Most often in SD and spontaneously hypertensive (SHR) strains
307
gross lesions of Polyarteritis nodosa
Thick, tortuous gray to red, hard, medium-zied muscular arteries
***spares pulmonary arteries, large arteries, and glomeruli
Focal hemorrhage
May have aneurysmal dilatations
308
histopath lesions of Polyarteritis nodosa
Fibrinoid necrosis w/ neutropilic and mononuclear infiltration of the intima and media
309
Which rats are most susceptible to urolithiasis
Zucker diabetic fatty rats
310
What predisposes a rat to ringtail
Keratin defect
- low humidity (<25%)
- genetics
- low environmental temperature
- dehydration
- poor nutrition
311
histopath lesions of ringtail
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
treatment of ringtail
Topical application of lanolin was found to be beneficial in the tx of this dz
313
Effects of hypovitaminosis A
314
Effect of Hypovitaminosis E
testicular degeration
315
Effect of hypovitaminosis K
Widespread hemorrhage due to loss of vitamin K-dependent coagulation factors (II, VII, IX, and X plus proteins C, S, and Z)
