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2

What agent is a gram negative, pleomorphic bacterium lacking a cell wall?

Mycoplasma pulmonis

3

2. Differential diagnoses for weight loss, piloerection, chattering, dyspnea, and torticollis

Mycoplasma pulmonis, CAR bacillus, Sendai virus, Pneumonia virus of mice, Corynebacteria kutscheri, Pneumocystis carnii

4

3. T/F Ooprhoritis, salpingitis, and metritis are seen in natural infections of Mycoplasma pulmonis.

False: has only been seen in experimental infection with this agent.

5

4. M. pulmonis can be found in approximately what percentage of conventional mouse colonies?

15%

6

5. How is M. pulmonis is spread?

Aerogenically

7

6. T/F  M. pulmonis can be transmitted in utero in mice

False-- demonstration of in utero tramsmission has only been seen in rats

8

7. T/F Mice infected with other pathogens are at increased risk of developing MRM

True--mice infected with Sendai or Mouse Coronavirus are at increased risk of developing MRM.

9

8. M. pulmonis has not been isolated from which of the following ?
a. Rat
b. Hamster
c. Gerbil
d. Guinea pig
e. Rabbit

C. Gerbil

10

9. T/F M. pulmonis in an intracellular organism.

False--extracellular

11

10. Where does M. pulmonis colonize?

Colonizes in the apical cell membranes of the respiratory epithelium anywhere between the anterior nasal passages to alveoli

12

11. M. pulmonis may injure host cells via what mechanism(s)?

1) Competition for metabolites (carbohydrates and metabolites)
2) Release of toxic substances (such as peroxides)

13

M. pulmonis causes ciliostasis, which leads to distrupted mucociliary transport.

True

14

13. How does Mycoplasma pulmonis interfere with research?

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

14. T/F Arthritis a significant feature of natural M. pulmonis infection

False

16

15. What strain(s) are resistant to pathogenic infection by M. pulmonis?

C57BL/6

17

16. T/F Lymphoid infiltration of the submucosa in the trachea can persist for weeks after initial infection with M. pulmonis.

True

18

17. What is the initial lesion of MRM (murine respiratory mycoplasmosis)?

Suppurative rhinitis

19

18. T/F Squamous metaplasia is a feature of MRM.

True

20

19. Pulmonary lesions in MRM are typified by?

bronchopneumonia spreading from the hilus

21

20. What are typical inflammatory lesions seen in MRM pneumonia?

Lymphoid and plasma cells around the bronchi with neutrophils in the bronchial lumen

22

21. The predominant lesions seen in chronic MRM include:

Suppurative bronchitis, bronchiolitis, and alveolitis

23

22. Serologic tests do not differentiate between which species of mycoplasmosis?

M. arthriditis and M. pulmonis

24

23. What is the media of choice for collecting samples for culture of M. pulmonis?

lavage with buffered saline or mycoplasma broth

25

24. Speciation of Mycoplasma species can be accomplished using what techniques?

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