BB Ch3 80-93 KD Flashcards
2
Q
What agent is a gram negative, pleomorphic bacterium lacking a cell wall?
A
Mycoplasma pulmonis
3
Q
- Differential diagnoses for weight loss, piloerection, chattering, dyspnea, and torticollis
A
Mycoplasma pulmonis, CAR bacillus, Sendai virus, Pneumonia virus of mice, Corynebacteria kutscheri, Pneumocystis carnii
4
Q
- T/F Ooprhoritis, salpingitis, and metritis are seen in natural infections of Mycoplasma pulmonis.
A
False: has only been seen in experimental infection with this agent.
5
Q
- M. pulmonis can be found in approximately what percentage of conventional mouse colonies?
A
15%
6
Q
- How is M. pulmonis is spread?
A
Aerogenically
7
Q
- T/F M. pulmonis can be transmitted in utero in mice
A
False– demonstration of in utero tramsmission has only been seen in rats
8
Q
- T/F Mice infected with other pathogens are at increased risk of developing MRM
A
True–mice infected with Sendai or Mouse Coronavirus are at increased risk of developing MRM.
9
Q
- M. pulmonis has not been isolated from which of the following ?
a. Rat
b. Hamster
c. Gerbil
d. Guinea pig
e. Rabbit
A
C. Gerbil
10
Q
- T/F M. pulmonis in an intracellular organism.
A
False–extracellular
11
Q
- Where does M. pulmonis colonize?
A
Colonizes in the apical cell membranes of the respiratory epithelium anywhere between the anterior nasal passages to alveoli
12
Q
- M. pulmonis may injure host cells via what mechanism(s)?
A
1) Competition for metabolites (carbohydrates and metabolites)
2) Release of toxic substances (such as peroxides)
13
Q
M. pulmonis causes ciliostasis, which leads to distrupted mucociliary transport.
A
True
14
Q
- How does Mycoplasma pulmonis interfere with research?
A
1) greater risk during general anesthesia
2) mitogenic for T and B lymphocytes
3) increase NK cell activity
4) contaminate cell lines and translatable tumors
15
Q
- T/F Arthritis a significant feature of natural M. pulmonis infection
A
False
16
Q
- What strain(s) are resistant to pathogenic infection by M. pulmonis?
A
C57BL/6
17
Q
- T/F Lymphoid infiltration of the submucosa in the trachea can persist for weeks after initial infection with M. pulmonis.
A
True
18
Q
- What is the initial lesion of MRM (murine respiratory mycoplasmosis)?
A
Suppurative rhinitis
19
Q
- T/F Squamous metaplasia is a feature of MRM.
A
True
20
Q
- Pulmonary lesions in MRM are typified by?
A
bronchopneumonia spreading from the hilus
21
Q
- What are typical inflammatory lesions seen in MRM pneumonia?
A
Lymphoid and plasma cells around the bronchi with neutrophils in the bronchial lumen
22
Q
- The predominant lesions seen in chronic MRM include:
A
Suppurative bronchitis, bronchiolitis, and alveolitis
23
Q
- Serologic tests do not differentiate between which species of mycoplasmosis?
A
M. arthriditis and M. pulmonis
24
Q
- What is the media of choice for collecting samples for culture of M. pulmonis?
A
lavage with buffered saline or mycoplasma broth
25
Q
- Speciation of Mycoplasma species can be accomplished using what techniques?
A
immunofluorescence, immunoperoxidase staining, growth inhibition, or PCR
26
25. T/F Treatment with tetracyclines is an effective means to eradicate M. pulmonis
False -- suppresses clinical disease but does not eliminate infection
27
27. T/F Natural infection by M. arthriditis can lead to arthritis.
False: nonpathogenic during natural infection; arthritogenic only after IV inoculation
28
Name clinical signs seen wtih natural infection:
Cilia-associated respiratory (CAR) bacillus
Clostridium piliforme
M. arthriditis
M. collis
M. pulmonis
CAR bacillus = chronic respiratory disease (rare)
Clostridium piliforme = diarrhea and inactivity and sudden death
M. arthriditis = nonpathogenic
M. collis = nonpathogenic
M. pulmonis = chattering, dyspnea, torticollis
29
Match the organism to the clinical signs seen with experimentally induced disease:
M. arthriditis
M. neurolyticum
M. pulmonis
M. arthriditis = arthritis
M. neurolyticum = spasmodic hyperextension of the head and rasigin of one foreleg followed by intermittent rolling on the long axis of the body
M. pulmonis = oophoritis, salpingitis, metritis
30
30. The etiologic agent of “rolling disease” is
Mycobacterium neurolyticum
31
31. What is the gram morphology of CAR bacillus?
Slender, gram negative bacillus
32
32. Describe clinical presentation of CAR bacillus in mice and rats.
Rats: clinical disease resembling MRM
Mice: natural infection is rare; appears to be more if an opportunistic pathogen, in co-infection with Sendai virus and/or PVM
33
33. Diagnosis of infection with CAR-bacillus can be done using what techniques:
ELISA or PCR for serological detection of infection
Histologically by staining with Warthrin-Starry (or similar stains) to visualize argyrophilic bacilli adhered to apical membranes of bronchial respiratory epithelium.
34
34. A histologic section of lung was stained with a Warthin-Starry stain. Argyrophilic bacilli were adherent to the apical membranes of bronchial respiratory epithelium. The most likely etiologic agent is
CAR bacillus
35
35. Sulfamerazine (500mg/liter) in drinking water may be effective in eradicating what organism
CAR bacillus
36
36. The etiologic agent of Tyzzer’s disease is
Clostridium piliforme
37
38. The gram morphology of Clostridium piliforme is
long, thin, gram negative, spore-forming bacterium
38
39. Tyzzer’s disease is named for
Ernest Tyzzer, first described in a colony of Japanese Waltzing mice
39
40. T/F C. piliforme can be successfully grown on cell-free media.
False
40
41. C. piliforme can be grown successfully by inoculation of :
susceptible vertebrates, yolk sac of embryonated eggs, hepatocytes cultures from mice
41
42. T/F Outbreaks of C. piliforme are usually explosive and have high mortality.
True
42
43. What clinical signs are usually seen with C. piliforme infection?
Unexpected deaths preceded by diarrhea and inactivity. Outbreaks can be explosive with high mortality. Subclinical infection may occur accompanied by antibody formation.
43
44. What conditions have been shown to predispose mice to Tyzzer’s disease
Overcrowding, High humidity, High temperature, Host genotype, Immunosuppression, Moist food
44
45. Which mouse is more resistant to Tyzzers, C57BL/6 or DBA/2?
C57BL/6
45
46. Depletion of what cell types have been shown to cause increased susceptibility to Tyzzer's disease?
T cells, B lymphocytes, neutrophils, NK cells
46
What is the reservoir of Tyzzer’s disease?
it is unknown
47
T/F Strains of C. piliforme are always host specific.
False, some strains can infect multiple hosts (mice, rats, hamsters)
48
49. Spores of C. piliforme can remain viable in the environment at room temperature for how long?
12 months
49
50. Which form (vegetative or spore) of C. piloforme should be considered the primary means of spread.
Spore form
50
51. The most likely source of environmental contamination of Tyzzer’s disease is
Feces contaminated food and soiled bedding
51
52. The mode of transmission of C. piliforme is
Fecal-oral
52
53. Infection with C. piliforme begins in the _______and spreads to the ____________ .
Intestines and spreads to the liver and heart
53
54. Lesions caused by C. piliforme are characterized by
Necrosis in the intestines, liver, heart, and mesenteric lymph nodes
54
55. During the necropsy of a mouse, it is noted that segments of the ileum, cecum, and colon are red and dilated, and contain watery, fetid contents. The liver contains gray-white foci. Based on these findings, differential diagnoses include
Salmonellosis, Tyzzer's Disease
55
56. Inflammation found in cases of Tyzzer’s disease is generally characterized as
Lymphocytic, and neutrophilic
56
57. T/F Bundles of long slender rods in the nucleus of dead cells bordering necrotic foci in the liver are diagnostic for Tyzzer’s disease.
False--they are in the cytoplasm
57
58. The stains most useful for diagnosing Tyzzer’s disease are
Silver Stains (Warthin-Starry), Giemsa, Periodic-Acid-Schiff
58
59. T/F Asymptomatic infections caused by Tyzzer’s disease can be detected by ELISA.
True; also by PCR
59
60. The causative agent of Transmissible Murine Colonic Hyperplasia is
Citrobacter rodentium
| Nonmotile, Gram-negative rod that ferments lactose but does not utilize citrate to a significant degree
60
62. The gram morphology of C. rodentium is
Gram negative rod
61
63. C. rodentium can/cannot ferment lactose.
C. rodentium can ferment lactose
62
64. C. rodentium can/cannot utilize citrate.
It does not utilize citrate or does so marginally
63
65. Clinical infection with Citrobacter rodentium is characterized by
rectal prolapse
| soft feces
64
66. Which age groups are more likely to develop Transmissible Murine Colonic Hyperplasia?
Suckling or recently weaned mice
65
67. T/F Citrobacter rodentium can be found in the GI flora of normal mice
False
66
68. C. rodentium can be spread by
Contact, Fecal-oral transmission
67
69. Which strain(s) of mice is(are) relatively resistant to infection with C. rodentium
DBA, C57BL, NIH Swiss
68
70. T/F Diet has no effect on infection by C. rodentium.
False; however, no specific dietary factor has been identified
69
71. Where does C. rodentium attach?
Mucosa of descending colon
70
72. The characteristic gross finding seen in Transmissible Murine Colonic Hyperplasia are:
Severe thickening of the descending colon
71
73. Lesions caused by C. rodentium persist how long?
For a few weeks
72
74. The agar of choice for identifying C. rodentium in culture is:
MacConkey's agar
73
75. What is the gram morphology of Pseudomonas aeruginosa?
Motile gram negative rod
74
76. What are typical clinical signs of infection with Pseudomonas aeruginosa
Almost always silent in immunocompetent mice.
Generalized infection is associated with severe leukopenia.
Immunocompromised mice prone to septicemia. Can cause severe or lethal infection in athymic mice. Sick mice can have equilibrium disturbances, conjunctivitis, serosanguinous nasal discharge, edema of head, weight loss, skin infections, GI ulcers
75
77. The most common clinical sign seen in immunocompetent mice infected with Pseudomonas aeruginosa is
subclinical
76
78. T/F Pseudomonas aeruginosa is part of the normal flora
False
77
79. Once established in a mouse, Pseudomonas aeruginosa can be found in what sites, which serve for further environmental contamination or direct transmission?
Nasopharynx, oropharynx, GI tract
78
T/F Pathogenic infection with Pseudomonas aeruginosa is most common in immunocompetent mice
False
79
81. Describe the pathogenesis in an immunodeficient mouse infected with Pseudomonas aeruginosa:
enters URT or gingiva --> bacteremia --> Necrosis of liver, spleen, or other tissues
80
82. On necropsy of an immunosuppressed mouse with clinical signs of weight loss, conjunctivitis, serosanguinous nasal discharge, and otitis media, you observe: bowel is distended with fluid, gastrointestinal ulceration is present, and the tympanic bulla contain green suppurative exudate. What is the most likely etiologic agent?
Pseudomonas aeruginosa
81
How can Pseudomonas aeruginosa carrier mice be identified?
by either nasal culture or by placing bottles of sterile, nonacidified, nonchlorinated water on cages for 24-48 hours and then culturing the sipper tubes
82
Acidification or hyperchlorination of the drinking water will eliminate established infection with Pseudomonas aeruginosa.
False - it can prevent infection but not eliminate established infections
83
85. Describe morphology of Pasteurella pneumotropica.
short, Gram-negative rod
84
Describe typical clinical signs and epizootiology of Pasteurella pneumotripica.
Usually asymptomatic. Opportunistic. Ubiquitous inhabitant of skin, upper respiratory tract, GI tract. Litters from infected dams can become infected during first week after birth.
85
T/F Pasteurella pneumotripica is most properly viewed as an opportunistic pathogen.
True
86
T/F Studies of experimental infections with Pasteurella pneumotropica suggest that it does not complicate pneumonias due to M. pulmonis and Sendai virus.
False, studies have shown that P. pneumotropica may complicate pneumonias due to M. pulmonis and Sendai virus
87
89. Pasteurella pneumotripica is a ubiquitous inhabitant of what sites in the mouse:
GI tract, Skin, Upper respiratory tract
88
90. How soon after birth can litters from dams infected with Pasteurella pneumotropica can become infected?
during the first week after birth
89
91. Describe the pathology associated with P. pneumotropica.
Suppurative inflammation, which may include abscessation, dermatitis, conjunctivitis, dacryoadenitis, panophthalmitis, mastitis, and infections of bulbourethral gland. Preputial and orbital abscesses can also occur, especially in athymic mice.
90
92. T/F Cutaneous lesions caused by P. pneumotropica are always associated with systemic disease.
False, cutaneous lesions can occur without systemic disease
91
93. Lesions caused by P. pneumotropica are most often
suppurative
92
94. T/F Infection with P. pneumotropica can be detected by ELISA
True
93
95. List 6 bacteria that can cause suppurative lesions in mice.
```
Pasteurella pneumotropica
Staphylococcus
Streptococcus
Corynebacterium
Klebsiella
Mycoplasma
```
94
96. What is the gram morphology of Helicobacter?
gram negative, curved to spiral shaped, microaerophilic
95
97. T/F Helicobacter can be grown in culture
True
96
98. Describe the environmental conditions under which Helicobacter can be grown in culture.
microaerobic atmosphere (5% CO2, 90% N2, 5% H2)
97
99. 2 types of media on which Helicobacter can be grown are:
freshly prepared antibiotic impregnated blood agar , or broth supplemented with fetal bovine serum
98
100. Helicobacter species isolated from mice include (hint, there are 6).
```
H. bilis
H. hepaticus
H. muridarum
H. rappini
H. rodentium
H. typhlonius
```
99
101. Regarding urease, catalase, and oxidase, Helicobacter organisms are most commonly:
urease positive
catalase positive
oxidase positive
100
102. List 2 species of Helicobacter that are urease negative.
H. rodentium and H. typhlonicus are urease negative
101
103. T/F Infection of adult immunocompetent mice with Helicobacter hepaticus usually causes inflammatory bowel disease.
False: infection in immunocompetent mice is usually asymptomatic. A/J mice can develop a typhlitis.
102
104. Liver lesions from helicobacters may increase susceptibility to _____________ among _____________ of the strains __________________.
Hepatomas and hepatocellular carcinomas, aged male mice, A/JCr and B6C3F
Also, hepatic hemangiosarcomas in B6C3F1.
This susceptibility has a dominant inheritance.
103
Which strains are susceptible to helicobacter hepatitis and which are resistant?
Susceptible: A/JCr, C3H/HeNCr, SJL/NCr
Resistant: C57BL/6
104
106. T/F H. hepaticus cannot persist in the GI tract (cecum and colon).
False: H. hepaticus CAN persist in the GI tract, in particular the cecum and the colon. This implies that carrier mice can spread infection in enzootically infected colonies.
105
107. T/F Proliferative typhlitis caused by H. hepaticus is always associated with liver lesions.
False: proliferative typhlitis, colitis, and proctitis can occur without coincident hepatitis
106
108. T/F Inflammation in the livers of mice infected with H. hepaticus originates in the central lobular areas of the liver and spreads to the portal triads.
False: inflammation orginates in the portal triads and spreads to the hepatic parenchyma
107
109. Histologically, liver lesions caused by H. hepaticus are characterized as:
Angiocentric nonsuppurative hepatits and hepatic necrosis
108
T/F H. hepaticus may cause necrosis in the liver of susceptible mice
True
109
111. Which strains of mice are susceptible to developing age-related hepatomas and hepatocellular carcinomas caused by H. hepaticus?
A/JCr and B6C3F1
110
112. Which strain of mice is resistant to hepatitis caused by H. hepaticus?
C57BL6
111
113. In which strain of mice infected with H. hepaticus is there an increased incidence of hepatic haemangiosarcoma?
B6C3F1
112
114. What is the pattern of inheritance for susceptibility to H. hepaticus-induced neoplasia?
dominant pattern of inheritance
113
115. T/F PCR can differentiate between H. hepaticus, H. bilis, H. ‘typhlonicus’, H muridarum and H. rappini.
False: PCR cannot differentiate between species; however, molecular speciation can be accomplished by restriction fragment length polymorphism analysis of the PCR product
114
116. T/F Helicobacters grow rapidly in culture, and no growth after 4 days is long enough to deem the culture “negative”.
False: Helicobacters require prolonged incubation (up to 3 weeks) in culture before it can be deemed negative.
115
117. H. bilis has been isolated from the livers and intestines of aged mice.
True
116
118. H. bilis induces what disease in SCID mice.
Inflammatory Bowel Disease
117
119. Name disease with each.
a. H. bilis
b. H. bilis and H. rodentium
c. H. muridarum
d. H. "rappini"
e. H. rodentium
f. H. typhlonicus
H. bilis = IBD in SCID
H. bilis and H. rodentium = natural outbreak of IBD in immunocompromised mice
H. muridarum = gastritis under certain circumstances
H. rappini = no clinical signs
H. rodentium = may be component of normal flora
H. typhlonicus = IBD in SCID
118
120. Match the bacteria with the site of isolation (some will have more than one answer)
a. H. bilis
b. H. muridarum
c. H. "rappini"
d. H. rodentium
H. bilis = liver and intestine
H. muridarum = ileum, cecum, colon, stomach
H. rappini = feces
H. rodentium = intestine
119
The combination of antibiotics most effective in treating infections with Helicobacter:
Triple therapy, daily gavage: amoxicillin, metronidazole, bismuth
120
122. What is the gram morphology of Corynebacterium bovis?
Short, gram postive rods
121
123. The etiologic agent of pseudotuberculosis in mice:
Corynebacterium kutcheri
122
124. T/F Corynebacterium kutscheri infection is often symptomatic in otherwise healthy mice
False--usually asymptomatic in otherwise healthy mice
123
125. T/F Active disease caused by C. kutscheri is precipitated by immunosuppression or environmental stress.
True
124
126. T/F Active disease caused by C. kutscheri is expressed as an acute illness with low mortality or a chronic syndrome with high mortality.
False: Active disease caused by C. kutscheri is expressed as an acute illness with HIGH mortality or a chronic syndrome with LOW mortality
125
127. Infection with C. bovis causes
Hyperkeratitic dermatitis, especially in immunodeficient muce
126
128. T/F Rats are susceptible to infection with C. kutscheri
True
127
What clinical manifestations are seen with mice infected with C. kutscheri?
Often asymptomatic in otherwise health mice. Active disease is precipitated by immunosuppressive or environmental stress: acute illness with high mortality or a chronic syndrome with low mortality.
128
130. What is the pathogenesis of C. kutscheri?
Asymptomatic mice thought to harbor organisms in upper alimentary tract, colon, and/or respiratory tract and regional lymph nodes. Transmission unclear but could be by multiple routes. Hematogenous spread to various organs, appearing as white nodules in kidney, liver, lung, and other sites. Septic, necrotic lesions often contain caseous material or liquified pus.
129
131. T/F Corynebacterium kutscheris is a primary skin pathogen
False: skin ulcers or fistulas follow bacterial embolization and infarcation of dermal vessels
130
132. Skin scaliness and alopecia is characterized by infection with which organism
Corynebacterium bovis
131
133. Nodular, caseous lesions are observed in the lung of a mouse. Which stains should be done to differentiate the etiologic agents?
Acid fast to rule out Mycobacterium avium and gram stain to rule out Corynebacterium kutscheri
132
134. T/F Scaly skin in glabrous mice can be caused by low humidity.
True
133
135. The gram morphology of Streptobacillus moniliformis:
nonmotile, gram negative, pleomorphic rod
134
136. What is the virulent form of Streptobacillus moniliformis
Bacillus form
135
137. T/F Streptobacillosis has an acute phase with high mortality, followed by a subacute phase, and finally a chronic phase that may persist for months.
True
136
138. What are the signs of acute disease with Streptobacillus moniliformis? Chronic disease?
Acute disease: Dull, damp hair coat and keratoconjunctivitis. Variable signs include anemia, diarrhea, hemoglobinuria, cyanosis, emaciation.
Chronic disease: cutaneous ulceration, arthritis, gangrenous amputation, arthritis can leave joints deformed and ankylosed. Hindlimb paralysis with urinary bladder distension, nicotine nice, kyphosis, and priaprism may occur if vertebral lesions impinge on motor nerves. Breeding mice may have stillbirths.
137
139. T/F Infection with Streptobacillus moniliformis can cause abortions and stillbirths.
True
138
140. The most likely source of dissemination of Streptobacillus moniliformis to mice in a laboratory animal setting is:
Asymptomatic persistently infected rats
139
141. The etiologic agent of rat bite fever in humans is:
Streptobacillus moniliformis
140
142. T/F Streptobacillus moniliformis has been isolated from joint fluid as long as 26 months after infection.
True
141
143. What is the appropriate culture media for Streptobacillus moniliformis from chronic lesions?
serum-enriched medium
142
144. Which antibiotics are an effective means to control of Streptobacillus moniliformis?
None
143
145. There are approximately 2400 known serotypes of Salmonella. What are the most common isolates from mice?
Salmonella enteritidis and Salmonella typhimurium
144
146. The gram morphology of Salmonella enteritidis:
gram negative rod
145
147. Does Salmonella enteritidis ferment lactose?
Rarely
146
148. Clinical signs that characterize acute, subacute, chronic, and enzootic salmonellosis?
Acute: especially severe in young mice; anorexia, weight loss, lethargy, dull coat, hunched posture, possibly conjunctivitis. Gastroenteritis is common but stool may remain formed.
Subacute: distended abdomens from hepatomegaly and splenomegaly.
Chronic: anorexia, weight loss
Enzootic: episodic, with alternating quiescence and high mortality with diarrhea, anorexia, weight loss, rough coat, reduced production
147
149. T/F Chronic infection with Salmonella enteritidis can produce distended abdomens from hepatomegaly and splenomegaly.
False: subacute infection can produce distended abdomens from hepatomegaly and splenomegaly
148
150. What are clinical signs suggestive of infection of Salmonella enteritidis in a breeding colony?
Alternating periods of quiescence and high mortality, anorexia, diarrhea, reduced production, weight loss
149
151. List potential sources of Salmonella infection.
Birds, Cats, Dogs, Feral rodents, Humans, Nonhuman primates, and Vermin can all serve as carriers
150
152. T/F Murine salmonellosis does not present a zoonotic hazard to humans.
False
151
153. T/F Adult mice are more susceptible to infection with Salmonella than weanling mice.
False: suckling and weanling mice are more susceptible than mature mice.
152
154. How does dietary iron intake affect severity of disease caused by Salmonella?
nutritional iron deficiency attentuates salmonella infection, whereas iron overload promotes bacterial growth and virulence factors
153
155. Describe the pathogenesis of Salmonella.
Penetrates intestinal wall --> Peyer's patches --> mesenteric lymph nodes --> bacteremia --> spleen and liver
154
156. T/F Salmonella enterititis infection has not been associated with chronic arthritis.
False: it has been associated with arthrtitis
155
157. Mice infected with Salmonella that survive for several weeks may have what gross lesions?
Intestines distended and reddened, liver and spleen enlarges with yellow-grey foci of necrosis, affected lymph nodes enlarged, red, and focally necrotic. Focal inflammation can develop in many organs, including the myocardium.
156
158. T/F Thrombosis from septic arterial embolism (esp. in the liver) may occur during infection with Salmonella.
False
157
159. What is a characteristic pathology with Salmonella chronic infection?
Granulomatous lesions, especially in the liver
158
160. T/F During acute Salmonellosis, bacteria cannot be isolated from the blood.
False, during acute stages, bacteria can be isolated in the blood.
159
161. Which is a more reliable site for culturing Salmonella from asymptomatic mice, Feces or Mesenteric lymph nodes?
MLN as fecal shedding can be intermittent
160
162. T/F The use of agglutination tests is a reliable way to identify antibodies to Salmonella in the serum of infected mice.
False, serological cross-reactivity is common
161
163. Infectious differential diagnoses for Salmonellosis include (list 8) .
1. Tyzzer's dz
2. Pseudomoniasis
3. Corynebacteriosis
4. Murine colonic hyperplasia
5. Pasteurellosis
6. Coronavirus
7. Ectromelia virus
8. Reovirus
162
164. A noninfectious differential diagnosis for Salmonellosis:
Mesenteric lymphadenopathy
163
165. T/F Infection with Salmonella can be controlled by treating with sulfa antibiotics.
False: there is no evidence that treating with any antibiotic is beneficial
164
A colony of SCID mice has a 6-month history of low mortality. Mice develop inappetance, become emaciated, have a hunched posture and a rough hair coat. Some mice develop hyperpnea, an ocular discharge, cutaneous ulcerations, and arthritis. At necropsy, gray-white nodules can be seen in the liver and lung. Histologic lesions are characterized by coagulative or caseous necrosis bordered by intense neutrophilic infiltration. Colonies of gram-positive organisms are sometimes visible in caseous lesions. The most likely diagnosis is infection with:
Corynebacterium kutscheri
165
167. A mouse develops a dull, damp hair coat, keratoconjunctivitis, and cyanosis. Over time it becomes emaciated and develops cutaneous ulcers, arthritis, and gangrenous amputation. Histologic findings include purulent polyarthritis. A gram stain of joint fluid shows gram-negative, pleomorphic rods. The most likely etiologic agent is:
Streptobacillus moniliformis
166
168. A nude mouse develops scaly skin. Histologic findings of the skin include acanthosis and moderate hyperkeratosis. There is mild, nonsuppurative inflammation. Gram-positive organisms are visible in the hyperkeratotic layers. The most likely etiologic agent?
Corynebacterium bovis
167
169. A weanling mouse presents with anorexia, weight loss, lethargy, dull coat, humped posture and conjunctivitis. Feces is formed. During necropsy, visceral hyperemia, a pale liver, and catarrhal enteritis is observed. Histologically, necrotic foci are found in the intestine, mesenteric lymph nodes, liver, and spleen. Neutrophilic leukocytes and histiocytes are observed in the lymphoid tissues. Culture of the mesenteric lymph nodes yields gram negative rods. The most likely etiologic agent:
Salmonella enteritis (acute disease)
168
170. A SCID mouse presents with a rectal prolapse. During necropsy, it is found that the cecum and large bowel are thickened. Proliferative typhlitis, colitis, and proctitis are present. No lesions are found in the liver. A silver stain of the crypts of the lower bowel shows spiral and curved organisms. The most likely etiologic agent:
Helicobacter hepaticus or H. bilis
