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Bac T > Test 1 > Flashcards

Test 1 Flashcards

1
Q

what is the function of pili?

A

Adhesion Virulence Conjugation Facilitate identification (diagnosis)

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2
Q

What common bacteria utilizes Pili as a function of virulence?

A

E. coli

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3
Q

Name 2 functions of the bacterial plasmid

A

virulence factors antibiotic resistance genes can be transferred between bacteria

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4
Q

define a pathogen

A

an organism that causes disease in a normal host

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5
Q

define pathogenicity

A

the ability of an organism to cause disease in a immunocompetent host

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6
Q

define virulence

A

relative measure of pathogenicity

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7
Q

what is defined as, the number of bacteria needed to cause an infection in 50% of exposed animals

A

Infectious dose 50

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8
Q

MLD?

A

minimum lethal dose

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9
Q

what is the difference between apparent and inapparent infection

A

apparent infection is an infection with overt Dz (example canine ehrichiosis) inapparent infection is an infection without the presence of overt Dz (example normal microbiota)

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10
Q

what are the 4 events of almost every infectious DZ

A
  1. Encounter 2. Entry 3. Multiplication and spread (infection) 4. Damage (pathogenesis)
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11
Q

define the “ingress” mode of entry for a pathogen

A

when a pathogen enters without crossing an epithelial barrier

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12
Q

give 2 examples of pathogen independent methods where by an organism can gain entry through epithelial penetration

A

insect transmission catheters blood transfusion infected needle

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13
Q

what is the inoculum size, and why is it important?

A

The amount of pathogen that you are exposed to. the inoculum size is a prime determinant in the outcome of exposure

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14
Q

what is the advantage for Staphylococcus Aureus to lyse RBCs

A

they lysis of RBCs will release hemoglobin, there by gaining access to Iron that the body is sequestering from the bacteria via transferrin

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15
Q

how is streptococcus equi distributed throughout the body?

A

through the lymphatic system

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16
Q

what is an endotoxin

A

constitutive part of the gram negative cell wall

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17
Q

is an endotoxin part of a gram -, gram + bacteria? or both?

A

only a Gram -

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18
Q

Do exotoxins come from a Gram -, or Gram + bacteria, or both?

A

Both

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19
Q

how does streptococcus pneumoniae evade phagocytic engulfment?

A

the production of a capsule protects the bacteria from the phagosomes

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20
Q

by what means does Rickettsia spp. escape phagocytosis?

A

the production of phospholipase that lyses the phagosome membrane

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21
Q

what is immunopathology? and what are some examples?

A

it is when the immune system it’s self causes damage immune complexes granuloma formationo

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22
Q

what are some examples of granuloma forming Dz’s

A

Rhodococcal pneumonia tuberculosis Johne’s Dz R. equi

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23
Q

What are the two cell types that cannot be identified using a gram stain?

A

Mycobacteria, and Mycoplasma

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24
Q

what is the exotoxin that streptococci produces that allows it to spread through tissues?

A

hyaluronidase

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25
Q

what is the toxin that is produced by staphylococci that aids in lysing the cell

A

hemolysins

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26
Q

diphtheria toxin stops the movement of ________ on host cellular mRNA

A

ribosomes

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27
Q

what is the main cause of “travelers diarrhea” ?

A

Enterotoxigenic E. coli

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28
Q

C. tetani is an obligate __________ found in soil and feces

A

anaerobe

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29
Q

Tetansopasmin toxin ascends to the spinal cord via……..

A

retrograde axonal transport

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30
Q

Tetanospasmin causes rigid muscle ____________

A

contraction

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31
Q

C. tetani secretes ___________ that causes cell death and necrosis

A

tetanolysin (hemolysin)

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32
Q

define opisthotonus

A

from the greek word opisthen meaning “behind”, and tonos meaning tenssion, is a severe state of hyperextension

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33
Q

what species are the most susceptible to tetanus toxin?

A

Horse > human > dog > cat > bird

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34
Q

what is a toxoid?

A

inactivated toxin that induces antitoxin

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35
Q

what is an antitoxin

A

production of a specific antibody to a specific toxin following natural infection

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36
Q

if you have an animal with an active Dz from a toxin, would you treat with a toxoid? or an antitoxin?

A

antitoxin

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37
Q

clostridium botulinum is a gram _____ _____, and is an obligate ______

A

positive rod anaerobe

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38
Q

T or F C. botulinum can cause Dz without entering the host

A

True, just the toxin is required within the host to cause Dz

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39
Q

what mediates the botulism Dz, the bacteria? or the bacterial exotoxin?

A

the exotoxin

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40
Q

toxicoinfectious botulism is a rare form where th bacteria multiply in the _____________ then produce the toxin which is absorbed __________

A

intestinal tract systemically

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41
Q

shaker foal syndrome is caused by toxidoinfectious botulism, where the bacteria replicate within the __________, this is also known as___________

A

intestinal tract floppy baby syndrome

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42
Q

how does tetanus toxin and botulism toxin differ in the site of action

A

tetanus acts on the CNS botulism acts on the peripheral nerve endings

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43
Q

botulism causes __________ whereas tetanus causes _________

A

flaccidity rigidity

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44
Q

why is the big limitation on the antitoxin for botulism?

A

it can only inactivate toxins that have not been bound, has 0 effect on bound toxin

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45
Q

what is the risk of using antibiotics when facing Botulism Dz

A

you can destroy the normal flora in the intestional tract, allowing room for colonization of C. botulinum

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46
Q

T or F Toxoids can protect cross species

A

FALSE

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47
Q

T or F an endotoxin is an important component of all gram + bacteria

A

False, it is Gram -

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48
Q

define immunogenic

A

the ability to create an immune response

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49
Q

what component of the endotoxin does the body most commonly produce an antigen against?

A

the O antigen

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50
Q

why is the O antigen of an endotoxin so effective?

A

it will physically inhibit the ability of macrophages and neutrophils to phagocytose the bacteria

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51
Q

what role do bile acids play in microbiota endotoxin within the intestinal tract?

A

they will detoxify the endotoxins before they can be absorbed

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52
Q

what are some common Dz in animals that are due to endotoxins

A

coliform mastitis diarrhea pneumonia pleuritis

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53
Q

T or F Endotoxins are responsible for very little damage to the cell and surrounding tissue

A

True most of the damage stems from inflammatory mediators

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54
Q

endotoxins in low concentrations will activate _______ by the __________ pathway

A

compliment alternative

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55
Q

what is the result of endotoxins in ↑ concentrations?

A

endotoxic (hypovolemic) shock

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56
Q

what is the pathogenesis of hypovolemic shock in ↑ concentrations of endotoxins

A

Prostaglandin release leads to vasodilation → leukotrienes and cytokines lead to increased vascular permeability → stimulation of coagulation resulting in DIC

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57
Q

define endotoxemia

A

presence of endotoxin in the blood

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58
Q

define bacteremia

A

presence of viable bacteria in the blood

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59
Q

what is the difference between endotoxemia, bacteremia, and septicemia

A

endotoxemia = presence of endotoxin in the blood, but no viable bacteria bacteremia = presence of viable bacteria in the blood septicemia = bacteremia associated with clinical signs

60
Q

What pathogen causes disease in animals

A

ETEC E.Coli

61
Q

T or F ETEC causes damage to enterocytes and hemorrhage

A

False ETEC does not cause cell damage, hemorrhage, inflammation, or foul smelling feces.

62
Q

What Type of Diarrhea does ETEC cause?

A

Hypersecretory

63
Q

Where does ETEC attach in the intestine?

A

Small Bowl on the apical surface of the enterocytes

64
Q

T or F ETEC does not secrete enterotoxins

A

False ETEC secretes a Heat Labile and a Heat Stable enterotoxin

65
Q

What are 3 non-diarrheal E.Coli syndromes?

A

Cattle: coliform mastitis Chicken: Omphalitis (bac T infection of yolk sac Dog: UTI

66
Q

Salmonella will be gram positive or gram negative when stained?

A

Negative

67
Q

Define Facultative Anaerobe

A

It uses either oxidative phosphorylation or fermentation (Growth with or without oxygen)

68
Q

What are the two most common pathogens for food borne illness?

A

S.Typhimurium S.Enteritidis

69
Q

T Or F Salmonella is part of the normal GI Microbiota

A

False

70
Q

What is the most common source of contamination for Salmonella?

A

FECES, POop! 💩

71
Q

What host factors help prevent infection and disease of Salmonella?

A
  1. Reduction of viable challenge bacteria due to innate defenses 2. Inhibition of binding to target intestinal epithelial cells due to competition and anti microbial production by NORMAL flora
72
Q

What are 3 factors that PROMOTE successful Salmonella infection?

A
  1. Virulence of Serotype 2. High Challenge Dose 3. Host Susceptibility
73
Q

What is the Multiplication and Spread step for Salmonella?

A

Salmonella INVADES the intestinal epithelium -next they traverse the epithelial cell -finally they invade the lamina propria and progress to the messenger in lymph nodes and the bloodstream in lamina propria salmonella multiply and stimulate extensive migration of neutrophils and phagocytes into lamina propria. INFLAMMATION Macrophages eat bacteria Salmonella survives in the macrophage (lysosomal resistant, facultative intercellular pathogen)

74
Q

T or F To diagnosis chronic salmonella infection one only needs a Single fecal culture to be diagnosed.

A

False, you need multiple fecal samples because carriers may shed the virus only intermittently

75
Q

What type(s) of diarrhea does salmonella cause?

A

Malabsorption: Causes direct cellular damage and inflammation, thus meaning that there is a decrease in nutrient absorption, and cell death and HEMORRHAGE Exudative: inflammatory response leads to leakage Hypersecretion: Inflammatory mediators :prostaglandins and bradykinins) activate adenylate Cyclase which leads to secretion

76
Q

What are some differences between ETEC and Salmonella??

A
77
Q

Define gastroenteritis

A

a syndrome characterized by GI symptoms including nausea, vomiting, diarrhea, and abdominal discomfort

78
Q

Define diarrhea

A

abnormal fecal discharge characterized by frequent and or fluid stool

79
Q

Define dysentery

A

an inflammatory disorder of GI tract often accompanied with blood and pus in feces

80
Q

Define enterocolitis

A

Inflammation involving the mucosa of both small and large intestines

81
Q

E. coli is a ___________ anaerobe which means…….

A

facultative, and can grow with or without the presence of oxygen

82
Q

E. coli is an ______cellular bacteria

A

extracellular

83
Q

what are the 4 primary pathotypes of E. coli?

A

enterotoxigenic E. coli (ETEC) enteropathogenic E. coli (EPEC) enterohemorrhagic E. coli (EHEC) enteroinvasive E.coli (EIEC)

84
Q

define a pathotype

A

a group of strains of a single species that cause a common Dz using a common set of virulence factors

85
Q

define a serogroup

A

an antigenically distinct variety of serotype, based only on O (LPS) antigens

86
Q

define serotype

A

an antigenically distinct varient within a bacterial species

87
Q

T or F you are able to pridict pathogenicity based on the O, H, and K antigens on a given bacterial pathogen

A

False they are used to separate the bacteria into groups

88
Q

T or F ETEC is a part of the normal microbiota of most animals

A

True it is ubiquitous in the farm environment and is shed in feces.

89
Q

What receptor is required for ETEC to bind on epithelial cells?

A

CHO containing receptors

90
Q

This pathotype of E. coli is most common in neonates (less then 3 days old)

A

ETEC

91
Q

Why is ETEC only able to produce Dz the first few days of life

A

the intestinal receptors required for adhesion are only present in young animals

92
Q

ETEC cause a ____________ diarrhea.

A

hypersecretory

93
Q

what is the pathogenesis by which ETEC causes hypersecretory diarrhea

A

inhibits absorption of Na+ and Cl- in the villi, and ↑ secretion of Cl- in the crypts → hypersecretion

94
Q

T or F ETEC cause severe damage to bound epithelium

A

False there is no direct damage to the epithelium to which it is bound

95
Q

what is the gold standard test for diagnosis of ETEC

A

Multiplex PCR looking specifically for virulence factors

96
Q

how does EPEC differ then ETEC with respects to mucosal damage?

A

EPEC adheres to small bowel enterocytes and destroys the normal microvillar architecture. Cytoskeletal derangements are accompanied by an inflammatory response and diarrhea

97
Q

Shigells dysentery and which E. coli pathotype share a similar toxin?

A

EHEC (enterohemorrhagic E. coli)

98
Q

which pathotype of E. Coli affects 4-12 week old piglets, and has an extremely high mortality

A

VTEC, verotoxin producing E. coli Mortality can be as high as 90%

99
Q

what is the distinguishing feature of EHEC?

A

the production of Shiga Toxin

100
Q

Salmonella is a _________ anaerobe, and is a ___________ _______cellular bacteria

A

Facultative anaerobe Facultative intracellular

101
Q

what is the most important subspecies of salmonella among veterinary medicine

A

Salmonella enterica

102
Q

what are the most common food borne salmonellosis in the US

A

S. typhimurium S. enteritidis

103
Q

what is meant when stated that Salmonella is an obligate pathogen

A

it is not part of any animal’s normal microbiota.

104
Q

what is the primary route of salmonella infection?

A

ingestion of contaminated feed or water

105
Q

by what mechanism does salmonella survive phagocytosis

A

Salmonella is a facultative intracellular pathogen, so it can survive both inside and outside of a cell, it has an innate ability to resist lysosomal enzymes

106
Q

once systemic Salmonella will spread through the lymphatic system, in what cells, and where are the most common places for it to travel to

A

Persists in macrophages and will be found in the spleen, liver, and lymph nodes

107
Q

how would the diarrhea for salmonellosis be characterized

A

Malabsorption, exudation, and hypersecretion

108
Q

define leutolysis, and what Dz is it a common consequence of fetal infection?

A

degradation of the corpus leuteum at the end of the luteal phase of estrous caused by fetal infection of salmonells

109
Q

A calf is presented to you at 4 days old with severe dehydration, acute diarrhea, and Afebrile. What is the most likely pathogen

A

E. coli

110
Q

in this Dz, the pathogen will adhere to the mucosal cells, but does not cause any damage. It does however cause severe secretory diarrhea through an exotoxin that blocks the absorption of Na+ and Cl-.

A

E. coli

111
Q

this pathogen is know for producing bloody, foul, fibrin containing feces, depression, and fever. It typically affects neonates that are two weeks or older.

A

Salmonella

112
Q

this pathogen is know for causing dehydration, mucoid feces, chronic diarrhea, and weight loss. This typically will not effect animals less then 6 days old because of the incubation period. It causes malabsorption, villus atrophy, and may have hypersecretory diarrhea.

A

Cryptospordia

113
Q

What is the only obligate helminth transmitted pathogenic bacteria?

A

Salmon poisoning Disease (SPD)

caused by Neorickettsia Helminthoeca

114
Q

What is the vector and the host(s) for neorickettsia helminthoeca?

A

Vector: trematode (fluke)

Hosts: Snails (inhabit fresh and brackish waters), Fish (salmonid fish?), Mammals

115
Q

T or F

Neorickettsia Helminthoeca usually causes a systemic infection

A

True, it usually enters the blood and spread to other tissues such as lymph nodes, spleen, tonsils, thymus, liver, lungs, brain

116
Q

Which pathogen is the only obligate helminth transmitted pathogenic bacteria?

A

Neorickettsia helminthoeca

Salmon Poisoning Disease

117
Q

How does a dog get infected with N. Helminthoeca?

A

By ingesting the raw fish that is infected with the fluke, which then attaches to small intestinal mucosa of dog, and inoculates N. Helminthoeca

118
Q

N. Helminthoeca infects what inside its dead end host?

A

It initially infects intestinal epithelium and then sets up shop in monocytes/macrophages in intestinal lymphoid tissue.

119
Q

What damage is seen with neorickettsia Helmintheoca?

A

Cell Destruction: Lysis of mononuclear phagocytes, lymphadomegaly, splenomegaly, hepatitis, enterities (replication in peyer’s patches)

(also causes thrombocytopenia, lymphopenia)

120
Q

What are clinical signs of neorickettsia helminthoeca?

A

Fever, anorexia, weight loss, weakness depression, vomiting, diarrhea, and DEATH

121
Q

What type of diarrhea is seen with Neorickettsia Helminthoeca?

A

Yellowish and in small quantity, later in severe cases may become hemorrhagic

122
Q

How do you diagnosis neorickettsia helminthoeca?

A

Geographical area (pacific northwest)

History of accesss to raw fish

Clinical signs (non specific: fever, anorexia, weight loss, yellow–Red bloody diarrhea)

Hematologic findings in serum (non specific: thrombocytopenia, lymphopenia, elevated ALP (liver), eosinophilia (parasite infection))

Fecal float: see eggs 5-7 days after infection

Cytology: Intracytoplasmic rickettsial bodies in monocyes/macrophages

123
Q

How do you treat neorickettsia helminthoeca?

A

Give oral antibiotics: TETRACYLINES

Praziquantel: kills flukes

Supportive treatment

124
Q

What is the name of the organism that causes Potomac Fever in horses?

A

Neorickettsia Risticii

125
Q

What is the vector for neorickettsia risticii (potomac horse fever)?

A

N. Risticii infects a trematode (wormy) which then infects pleurocerid snalels and acuatic insects (caddis flies)

126
Q

T or F

Neorickettsia Risticii (Potomac Horse Fever) can be spread between horses

A

FALSE:

Infectious, but not contagious :)

127
Q

Where does Neorickettsia Risticii infect the host?

A

It infects monocytes and intestinal epithelial cells

Can become systemic

Cell entry: endocytosis into host vacuole

Cell Stages: MORULA-like inclusions seen in infected monocytes and intestinal epithelial cells

128
Q

What are the clinical signs for neorickettsia Risticii?

A

Non specifc: Fever, anorexia, depression (inflammatory response)

Specifc: infection of intestinal epithelium (typhocolitis) leading to SEVERE: colic, ileus, diarrhea, laminitis

Abortion is also possible

129
Q

T or F

Horses can become persistently infected by Neorickettsia Risticii AKA Potomac horse fever.

A

FALSE: Persistent infections are not recognized with this disease

130
Q

What diagnostic tests can you use to detect neorickettsia risticii?

A

Serology: IFA test (paired serum is confimatory)

paired serum since no persistence and they must be collected 3-5 days apart

may be confounded by vaccination

PCR: specific and sensitive

blood or tissues

131
Q

How do you treat neorickettsia risticii?

A

Tetracyclines

Supportive care: toxemia, dehydration

132
Q

What are the Clincial syndromes associated with Salmonella?

A
  1. Hemorrhagic Enterocolitis: characterized by inflammation in the lamina propria and submucosa
  • Diarrhea: mild–severe, fould smelling, watery, fibrin, mucous, blood and mucosal shreds (due to inflammation and exudate)
  • Dehydration
  • vomiting
  • fever

intestinal damage can lead to chronic weight loss: infection can result in fusion of regenerating villi during healing, leading to malabsorption

  1. Septicemia
    * this produces numberous clinical signs due to endotoxemia: DIC, infected mucous membranes, tachycardia, dry gangrene, pneumonia, meningitis, arthritis
  2. Abortion
  • Infection of fetus, causes relase of PGF2alpha causing luteolysis
    *
133
Q

T or F

Antibodies made in response to one serotype of salmonella will be cross protective to another serotype

A

FALSE: Antibodies are primarily directed towards o antigen side chain

134
Q

What type of immune response is important in controlling salmonella infection?

A

Cell-mediated immunity

macrophage activation mediates immune response

135
Q

How does salmonella cause carriers by persistent infection?

A

It escapes as an intracellular organism and is protected from ABs, antimicrobials, and complement

136
Q

Why can antibiotic treatment casue reactivation of a disease and shedding?

A

Because they alter the normal microflora

137
Q

What are the best ways to diagnosis salmonella?

A

Cytology: feces may contai neutrophils, erythrocytes

Isolation of salmonella is the gold standard

  • fecal samples (repeated 4-5 times)
  • Rectal biopsy and culture: ay provide better sensitivity
  • blood culture: useful in case of septicemia
  • dead animals: necropsy: intesting, spleen, liver, gall bladder, lymph node
138
Q

What species has the greatest zoonotic potential for salmonella?

A

DOGS and HORSES

(infants and the elderly are especially prone to infection)

139
Q

What is one conern with the use of antibiotics in the treatment of salmonella?

A

Antibiotic RESISTANCE

140
Q

Camplyobacter jejuni when gram stained will reveal what?

A

that it is gram negative slender, curved, motile ROD

141
Q

Which species are carriers of Campylobacter Jejuni?

A

Inapparent carriers: dogs, cats

apparent: Poultry (normal flora) WASH your raw chicken before cooking

142
Q

Disease severity in campylobacter jejuni is dependent upon what?

A

Inoculum size

Immune status: lack of previous exposure and development of protective AB

Concurrent infection: salmonella, parvovirus, coronavirus, etc. play a synergistic role in casuing disease.

Enbironmetal, physiologic, and surgical stress exacerate the disease

143
Q

What are two known ways that campylobacter jejuni causes disease?

A

Adhesions: probide attachement to and invasion of mucosal epithelial cells (jejunum, ileum, colon)

Prodces Cytotoxins: Cytolethal distending toxin

Destroys villi and induces inflammation

Invades epithelium

144
Q

What are the clinical signs for campylobacter jejuni?

A
  1. most commmonly there are no clinical signs
  2. can produce hemorrhagic gastroenteritis
  • most common in stressed animals less than 6 months old (wide spread diarrhea ranging from mild to watery to bloody)
  • presents similar to salmonella
  • can produce bacteremia
    • may see fever
145
Q

What is the best way to diagnosis campylobacter jejuni?

A

Fecal Culture is the gold standard.

Direct microscopic examination of feces usingwet mount (careful when interpreting results as other bacteria may look similar)

146
Q

How do you treat campylobacter jejuni?

A

FLUID THERAPY!!

antibiotics : efficacy not known in dogs and cats

severe cases may warrant antibitotic therapy: may reduce human exposure through reduced shedding

Antibiotic resistance is common

147
Q
A

Bac T (5 decks)

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