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Mice > BB Ch3 80-93 KD > Flashcards

BB Ch3 80-93 KD Flashcards

2
Q

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

A

Mycoplasma pulmonis

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3
Q
  1. 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

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4
Q
  1. 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.

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5
Q
  1. M. pulmonis can be found in approximately what percentage of conventional mouse colonies?
A

15%

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6
Q
  1. How is M. pulmonis is spread?
A

Aerogenically

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7
Q
  1. T/F M. pulmonis can be transmitted in utero in mice
A

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

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8
Q
  1. 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.

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9
Q
  1. 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

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10
Q
  1. T/F M. pulmonis in an intracellular organism.
A

False–extracellular

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11
Q
  1. Where does M. pulmonis colonize?
A

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

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12
Q
  1. 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)

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13
Q

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

A

True

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14
Q
  1. 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

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15
Q
  1. T/F Arthritis a significant feature of natural M. pulmonis infection
A

False

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16
Q
  1. What strain(s) are resistant to pathogenic infection by M. pulmonis?
A

C57BL/6

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17
Q
  1. T/F Lymphoid infiltration of the submucosa in the trachea can persist for weeks after initial infection with M. pulmonis.
A

True

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18
Q
  1. What is the initial lesion of MRM (murine respiratory mycoplasmosis)?
A

Suppurative rhinitis

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19
Q
  1. T/F Squamous metaplasia is a feature of MRM.
A

True

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20
Q
  1. Pulmonary lesions in MRM are typified by?
A

bronchopneumonia spreading from the hilus

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21
Q
  1. What are typical inflammatory lesions seen in MRM pneumonia?
A

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

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22
Q
  1. The predominant lesions seen in chronic MRM include:
A

Suppurative bronchitis, bronchiolitis, and alveolitis

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23
Q
  1. Serologic tests do not differentiate between which species of mycoplasmosis?
A

M. arthriditis and M. pulmonis

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24
Q
  1. What is the media of choice for collecting samples for culture of M. pulmonis?
A

lavage with buffered saline or mycoplasma broth

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25
Q
  1. Speciation of Mycoplasma species can be accomplished using what techniques?
A

immunofluorescence, immunoperoxidase staining, growth inhibition, or PCR

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26
Q
  1. T/F Treatment with tetracyclines is an effective means to eradicate M. pulmonis
A

False – suppresses clinical disease but does not eliminate infection

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27
Q
  1. T/F Natural infection by M. arthriditis can lead to arthritis.
A

False: nonpathogenic during natural infection; arthritogenic only after IV inoculation

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28
Q

Name clinical signs seen wtih natural infection:
Cilia-associated respiratory (CAR) bacillus
Clostridium piliforme
M. arthriditis
M. collis
M. pulmonis

A

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

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29
Q

Match the organism to the clinical signs seen with experimentally induced disease:
M. arthriditis
M. neurolyticum
M. pulmonis

A

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

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30
Q
  1. The etiologic agent of “rolling disease” is
A

Mycobacterium neurolyticum

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31
Q
  1. What is the gram morphology of CAR bacillus?
A

Slender, gram negative bacillus

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32
Q
  1. Describe clinical presentation of CAR bacillus in mice and rats.
A

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

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33
Q
  1. Diagnosis of infection with CAR-bacillus can be done using what techniques:
A

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.

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34
Q
  1. 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
A

CAR bacillus

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35
Q
  1. Sulfamerazine (500mg/liter) in drinking water may be effective in eradicating what organism
A

CAR bacillus

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36
Q
  1. The etiologic agent of Tyzzer’s disease is
A

Clostridium piliforme

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37
Q
  1. The gram morphology of Clostridium piliforme is
A

long, thin, gram negative, spore-forming bacterium

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38
Q
  1. Tyzzer’s disease is named for
A

Ernest Tyzzer, first described in a colony of Japanese Waltzing mice

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39
Q
  1. T/F C. piliforme can be successfully grown on cell-free media.
A

False

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40
Q
  1. C. piliforme can be grown successfully by inoculation of :
A

susceptible vertebrates, yolk sac of embryonated eggs, hepatocytes cultures from mice

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41
Q
  1. T/F Outbreaks of C. piliforme are usually explosive and have high mortality.
A

True

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42
Q
  1. What clinical signs are usually seen with C. piliforme infection?
A

Unexpected deaths preceded by diarrhea and inactivity. Outbreaks can be explosive with high mortality. Subclinical infection may occur accompanied by antibody formation.

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43
Q
  1. What conditions have been shown to predispose mice to Tyzzer’s disease
A

Overcrowding, High humidity, High temperature, Host genotype, Immunosuppression, Moist food

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44
Q
  1. Which mouse is more resistant to Tyzzers, C57BL/6 or DBA/2?
A

C57BL/6

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45
Q
  1. Depletion of what cell types have been shown to cause increased susceptibility to Tyzzer’s disease?
A

T cells, B lymphocytes, neutrophils, NK cells

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46
Q

What is the reservoir of Tyzzer’s disease?

A

it is unknown

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47
Q

T/F Strains of C. piliforme are always host specific.

A

False, some strains can infect multiple hosts (mice, rats, hamsters)

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48
Q
  1. Spores of C. piliforme can remain viable in the environment at room temperature for how long?
A

12 months

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49
Q
  1. Which form (vegetative or spore) of C. piloforme should be considered the primary means of spread.
A

Spore form

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50
Q
  1. The most likely source of environmental contamination of Tyzzer’s disease is
A

Feces contaminated food and soiled bedding

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51
Q
  1. The mode of transmission of C. piliforme is
A

Fecal-oral

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52
Q
  1. Infection with C. piliforme begins in the _______and spreads to the ____________ .
A

Intestines and spreads to the liver and heart

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53
Q
  1. Lesions caused by C. piliforme are characterized by
A

Necrosis in the intestines, liver, heart, and mesenteric lymph nodes

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54
Q
  1. 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
A

Salmonellosis, Tyzzer’s Disease

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55
Q
  1. Inflammation found in cases of Tyzzer’s disease is generally characterized as
A

Lymphocytic, and neutrophilic

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56
Q
  1. 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.
A

False–they are in the cytoplasm

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57
Q
  1. The stains most useful for diagnosing Tyzzer’s disease are
A

Silver Stains (Warthin-Starry), Giemsa, Periodic-Acid-Schiff

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58
Q
  1. T/F Asymptomatic infections caused by Tyzzer’s disease can be detected by ELISA.
A

True; also by PCR

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59
Q
  1. The causative agent of Transmissible Murine Colonic Hyperplasia is
A

Citrobacter rodentium

Nonmotile, Gram-negative rod that ferments lactose but does not utilize citrate to a significant degree

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60
Q
  1. The gram morphology of C. rodentium is
A

Gram negative rod

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61
Q
  1. C. rodentium can/cannot ferment lactose.
A

C. rodentium can ferment lactose

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62
Q
  1. C. rodentium can/cannot utilize citrate.
A

It does not utilize citrate or does so marginally

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63
Q
  1. Clinical infection with Citrobacter rodentium is characterized by
A

rectal prolapse

soft feces

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64
Q
  1. Which age groups are more likely to develop Transmissible Murine Colonic Hyperplasia?
A

Suckling or recently weaned mice

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65
Q
  1. T/F Citrobacter rodentium can be found in the GI flora of normal mice
A

False

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66
Q
  1. C. rodentium can be spread by
A

Contact, Fecal-oral transmission

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67
Q
  1. Which strain(s) of mice is(are) relatively resistant to infection with C. rodentium
A

DBA, C57BL, NIH Swiss

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68
Q
  1. T/F Diet has no effect on infection by C. rodentium.
A

False; however, no specific dietary factor has been identified

69
Q
  1. Where does C. rodentium attach?
A

Mucosa of descending colon

70
Q
  1. The characteristic gross finding seen in Transmissible Murine Colonic Hyperplasia are:
A

Severe thickening of the descending colon

71
Q
  1. Lesions caused by C. rodentium persist how long?
A

For a few weeks

72
Q
  1. The agar of choice for identifying C. rodentium in culture is:
A

MacConkey’s agar

73
Q
  1. What is the gram morphology of Pseudomonas aeruginosa?
A

Motile gram negative rod

74
Q
  1. What are typical clinical signs of infection with Pseudomonas aeruginosa
A

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
Q
  1. The most common clinical sign seen in immunocompetent mice infected with Pseudomonas aeruginosa is
A

subclinical

76
Q
  1. T/F Pseudomonas aeruginosa is part of the normal flora
A

False

77
Q
  1. Once established in a mouse, Pseudomonas aeruginosa can be found in what sites, which serve for further environmental contamination or direct transmission?
A

Nasopharynx, oropharynx, GI tract

78
Q

T/F Pathogenic infection with Pseudomonas aeruginosa is most common in immunocompetent mice

A

False

79
Q
  1. Describe the pathogenesis in an immunodeficient mouse infected with Pseudomonas aeruginosa:
A

enters URT or gingiva –> bacteremia –> Necrosis of liver, spleen, or other tissues

80
Q
  1. 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?
A

Pseudomonas aeruginosa

81
Q

How can Pseudomonas aeruginosa carrier mice be identified?

A

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
Q

Acidification or hyperchlorination of the drinking water will eliminate established infection with Pseudomonas aeruginosa.

A

False - it can prevent infection but not eliminate established infections

83
Q
  1. Describe morphology of Pasteurella pneumotropica.
A

short, Gram-negative rod

84
Q

Describe typical clinical signs and epizootiology of Pasteurella pneumotripica.

A

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
Q

T/F Pasteurella pneumotripica is most properly viewed as an opportunistic pathogen.

A

True

86
Q

T/F Studies of experimental infections with Pasteurella pneumotropica suggest that it does not complicate pneumonias due to M. pulmonis and Sendai virus.

A

False, studies have shown that P. pneumotropica may complicate pneumonias due to M. pulmonis and Sendai virus

87
Q
  1. Pasteurella pneumotripica is a ubiquitous inhabitant of what sites in the mouse:
A

GI tract, Skin, Upper respiratory tract

88
Q
  1. How soon after birth can litters from dams infected with Pasteurella pneumotropica can become infected?
A

during the first week after birth

89
Q
  1. Describe the pathology associated with P. pneumotropica.
A

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
Q
  1. T/F Cutaneous lesions caused by P. pneumotropica are always associated with systemic disease.
A

False, cutaneous lesions can occur without systemic disease

91
Q
  1. Lesions caused by P. pneumotropica are most often
A

suppurative

92
Q
  1. T/F Infection with P. pneumotropica can be detected by ELISA
A

True

93
Q
  1. List 6 bacteria that can cause suppurative lesions in mice.
A 
Pasteurella pneumotropica	
Staphylococcus	
Streptococcus	
Corynebacterium	
Klebsiella	
Mycoplasma
94
Q
  1. What is the gram morphology of Helicobacter?
A

gram negative, curved to spiral shaped, microaerophilic

95
Q
  1. T/F Helicobacter can be grown in culture
A

True

96
Q
  1. Describe the environmental conditions under which Helicobacter can be grown in culture.
A

microaerobic atmosphere (5% CO2, 90% N2, 5% H2)

97
Q
  1. 2 types of media on which Helicobacter can be grown are:
A

freshly prepared antibiotic impregnated blood agar , or broth supplemented with fetal bovine serum

98
Q
  1. Helicobacter species isolated from mice include (hint, there are 6).
A 
H. bilis	
H. hepaticus	
H. muridarum	
H. rappini	
H. rodentium	
H. typhlonius
99
Q
  1. Regarding urease, catalase, and oxidase, Helicobacter organisms are most commonly:
A

urease positive
catalase positive
oxidase positive

100
Q
  1. List 2 species of Helicobacter that are urease negative.
A

H. rodentium and H. typhlonicus are urease negative

101
Q
  1. T/F Infection of adult immunocompetent mice with Helicobacter hepaticus usually causes inflammatory bowel disease.
A

False: infection in immunocompetent mice is usually asymptomatic. A/J mice can develop a typhlitis.

102
Q
  1. Liver lesions from helicobacters may increase susceptibility to _____________ among _____________ of the strains __________________.
A

Hepatomas and hepatocellular carcinomas, aged male mice, A/JCr and B6C3F
Also, hepatic hemangiosarcomas in B6C3F1.
This susceptibility has a dominant inheritance.

103
Q

Which strains are susceptible to helicobacter hepatitis and which are resistant?

A

Susceptible: A/JCr, C3H/HeNCr, SJL/NCr
Resistant: C57BL/6

104
Q
  1. T/F H. hepaticus cannot persist in the GI tract (cecum and colon).
A

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
Q
  1. T/F Proliferative typhlitis caused by H. hepaticus is always associated with liver lesions.
A

False: proliferative typhlitis, colitis, and proctitis can occur without coincident hepatitis

106
Q
  1. 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.
A

False: inflammation orginates in the portal triads and spreads to the hepatic parenchyma

107
Q
  1. Histologically, liver lesions caused by H. hepaticus are characterized as:
A

Angiocentric nonsuppurative hepatits and hepatic necrosis

108
Q

T/F H. hepaticus may cause necrosis in the liver of susceptible mice

A

True

109
Q
  1. Which strains of mice are susceptible to developing age-related hepatomas and hepatocellular carcinomas caused by H. hepaticus?
A

A/JCr and B6C3F1

110
Q
  1. Which strain of mice is resistant to hepatitis caused by H. hepaticus?
A

C57BL6

111
Q
  1. In which strain of mice infected with H. hepaticus is there an increased incidence of hepatic haemangiosarcoma?
A

B6C3F1

112
Q
  1. What is the pattern of inheritance for susceptibility to H. hepaticus-induced neoplasia?
A

dominant pattern of inheritance

113
Q
  1. T/F PCR can differentiate between H. hepaticus, H. bilis, H. ‘typhlonicus’, H muridarum and H. rappini.
A

False: PCR cannot differentiate between species; however, molecular speciation can be accomplished by restriction fragment length polymorphism analysis of the PCR product

114
Q
  1. T/F Helicobacters grow rapidly in culture, and no growth after 4 days is long enough to deem the culture “negative”.
A

False: Helicobacters require prolonged incubation (up to 3 weeks) in culture before it can be deemed negative.

115
Q
  1. H. bilis has been isolated from the livers and intestines of aged mice.
A

True

116
Q
  1. H. bilis induces what disease in SCID mice.
A

Inflammatory Bowel Disease

117
Q
  1. 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
A

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
Q
  1. 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
A

H. bilis = liver and intestine
H. muridarum = ileum, cecum, colon, stomach
H. rappini = feces
H. rodentium = intestine

119
Q

The combination of antibiotics most effective in treating infections with Helicobacter:

A

Triple therapy, daily gavage: amoxicillin, metronidazole, bismuth

120
Q
  1. What is the gram morphology of Corynebacterium bovis?
A

Short, gram postive rods

121
Q
  1. The etiologic agent of pseudotuberculosis in mice:
A

Corynebacterium kutcheri

122
Q
  1. T/F Corynebacterium kutscheri infection is often symptomatic in otherwise healthy mice
A

False–usually asymptomatic in otherwise healthy mice

123
Q
  1. T/F Active disease caused by C. kutscheri is precipitated by immunosuppression or environmental stress.
A

True

124
Q
  1. T/F Active disease caused by C. kutscheri is expressed as an acute illness with low mortality or a chronic syndrome with high mortality.
A

False: Active disease caused by C. kutscheri is expressed as an acute illness with HIGH mortality or a chronic syndrome with LOW mortality

125
Q
  1. Infection with C. bovis causes
A

Hyperkeratitic dermatitis, especially in immunodeficient muce

126
Q
  1. T/F Rats are susceptible to infection with C. kutscheri
A

True

127
Q

What clinical manifestations are seen with mice infected with C. kutscheri?

A

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
Q
  1. What is the pathogenesis of C. kutscheri?
A

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
Q
  1. T/F Corynebacterium kutscheris is a primary skin pathogen
A

False: skin ulcers or fistulas follow bacterial embolization and infarcation of dermal vessels

130
Q
  1. Skin scaliness and alopecia is characterized by infection with which organism
A

Corynebacterium bovis

131
Q
  1. Nodular, caseous lesions are observed in the lung of a mouse. Which stains should be done to differentiate the etiologic agents?
A

Acid fast to rule out Mycobacterium avium and gram stain to rule out Corynebacterium kutscheri

132
Q
  1. T/F Scaly skin in glabrous mice can be caused by low humidity.
A

True

133
Q
  1. The gram morphology of Streptobacillus moniliformis:
A

nonmotile, gram negative, pleomorphic rod

134
Q
  1. What is the virulent form of Streptobacillus moniliformis
A

Bacillus form

135
Q
  1. 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.
A

True

136
Q
  1. What are the signs of acute disease with Streptobacillus moniliformis? Chronic disease?
A

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
Q
  1. T/F Infection with Streptobacillus moniliformis can cause abortions and stillbirths.
A

True

138
Q
  1. The most likely source of dissemination of Streptobacillus moniliformis to mice in a laboratory animal setting is:
A

Asymptomatic persistently infected rats

139
Q
  1. The etiologic agent of rat bite fever in humans is:
A

Streptobacillus moniliformis

140
Q
  1. T/F Streptobacillus moniliformis has been isolated from joint fluid as long as 26 months after infection.
A

True

141
Q
  1. What is the appropriate culture media for Streptobacillus moniliformis from chronic lesions?
A

serum-enriched medium

142
Q
  1. Which antibiotics are an effective means to control of Streptobacillus moniliformis?
A

None

143
Q
  1. There are approximately 2400 known serotypes of Salmonella. What are the most common isolates from mice?
A

Salmonella enteritidis and Salmonella typhimurium

144
Q
  1. The gram morphology of Salmonella enteritidis:
A

gram negative rod

145
Q
  1. Does Salmonella enteritidis ferment lactose?
A

Rarely

146
Q
  1. Clinical signs that characterize acute, subacute, chronic, and enzootic salmonellosis?
A

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
Q
  1. T/F Chronic infection with Salmonella enteritidis can produce distended abdomens from hepatomegaly and splenomegaly.
A

False: subacute infection can produce distended abdomens from hepatomegaly and splenomegaly

148
Q
  1. What are clinical signs suggestive of infection of Salmonella enteritidis in a breeding colony?
A

Alternating periods of quiescence and high mortality, anorexia, diarrhea, reduced production, weight loss

149
Q
  1. List potential sources of Salmonella infection.
A

Birds, Cats, Dogs, Feral rodents, Humans, Nonhuman primates, and Vermin can all serve as carriers

150
Q
  1. T/F Murine salmonellosis does not present a zoonotic hazard to humans.
A

False

151
Q
  1. T/F Adult mice are more susceptible to infection with Salmonella than weanling mice.
A

False: suckling and weanling mice are more susceptible than mature mice.

152
Q
  1. How does dietary iron intake affect severity of disease caused by Salmonella?
A

nutritional iron deficiency attentuates salmonella infection, whereas iron overload promotes bacterial growth and virulence factors

153
Q
  1. Describe the pathogenesis of Salmonella.
A

Penetrates intestinal wall –> Peyer’s patches –> mesenteric lymph nodes –> bacteremia –> spleen and liver

154
Q
  1. T/F Salmonella enterititis infection has not been associated with chronic arthritis.
A

False: it has been associated with arthrtitis

155
Q
  1. Mice infected with Salmonella that survive for several weeks may have what gross lesions?
A

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
Q
  1. T/F Thrombosis from septic arterial embolism (esp. in the liver) may occur during infection with Salmonella.
A

False

157
Q
  1. What is a characteristic pathology with Salmonella chronic infection?
A

Granulomatous lesions, especially in the liver

158
Q
  1. T/F During acute Salmonellosis, bacteria cannot be isolated from the blood.
A

False, during acute stages, bacteria can be isolated in the blood.

159
Q
  1. Which is a more reliable site for culturing Salmonella from asymptomatic mice, Feces or Mesenteric lymph nodes?
A

MLN as fecal shedding can be intermittent

160
Q
  1. T/F The use of agglutination tests is a reliable way to identify antibodies to Salmonella in the serum of infected mice.
A

False, serological cross-reactivity is common

161
Q
  1. Infectious differential diagnoses for Salmonellosis include (list 8) .
A
  1. Tyzzer’s dz
  2. Pseudomoniasis
  3. Corynebacteriosis
  4. Murine colonic hyperplasia
  5. Pasteurellosis
  6. Coronavirus
  7. Ectromelia virus
  8. Reovirus
162
Q
  1. A noninfectious differential diagnosis for Salmonellosis:
A

Mesenteric lymphadenopathy

163
Q
  1. T/F Infection with Salmonella can be controlled by treating with sulfa antibiotics.
A

False: there is no evidence that treating with any antibiotic is beneficial

164
Q

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:

A

Corynebacterium kutscheri

165
Q
  1. 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:
A

Streptobacillus moniliformis

166
Q
  1. 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?
A

Corynebacterium bovis

167
Q
  1. 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:
A

Salmonella enteritis (acute disease)

168
Q
  1. 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:
A

Helicobacter hepaticus or H. bilis

Mice (20 decks)

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