Respiratory pathogens 1 (tesse) Flashcards

1
Q

Where is the ciliated epithelium in the resp tract

A

nasal epithelium
bronchi
trachea
pharynx (?)

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2
Q

what is the function of the ciliated epithelium

A

muco-ciliary apparatus

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3
Q

What are the three bacteria with tropism for the ciliated epithelium

A

Bordetella
Mycoplasma
Chlamydia

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4
Q

What are the three routes of infection into the respiratory tract

A

aerosol
particle/droplet
conjuctival

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5
Q

what determines the severity, type and location of respiratory infection

A

bacterial virulence factors

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6
Q

what are the types of respiratory infections

A

pharyngitis/laryngitis
tracheitis
bronchitis
pneumonia
etc

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7
Q

what virulence factors are responsible for Adherence and resistance to expulsion:

A
  • Pili (Fimbriae)
  • Adhesins
  • Biofilm
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8
Q

what virulence factors are responsible for Survival in infected cells:

A
  • Ability to compete for iron
  • Survival in phagosomes
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9
Q

what virulence factors are responsible for Invasion of host cells:

A
  • Adhesins type Invasins
  • Interaction with cytoskeleton to promote
    engulfment
  • M-protein for Streptococcus
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10
Q

what virulence factors are responsible for Disease production/damage host:

A
  • Super antigens
  • Cell wall components
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11
Q

What are the main resp pathogens of cattle

A

Mannheimia haemolytica
Pasteurella multocida
Bibersteinia trehalosi
Histophilus somni
Mycoplasma bovis
Mycobacterium bovis

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12
Q

what is shipping fever

A

combination of primary or secondary bacterial pathogens with primary or secondary viral pathogens and stress

(virus + bacteria + stress)

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13
Q

etiology of Mannheimia haemolytica

A
  • Gram-negative, pleomorphic rod/coccobacilli
  • Related to Pasteurella (formerly Pasteurella haemolytica)
  • Fastidious
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14
Q

Mannheimia haemolytica is commensal to the

A

oropharynx

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15
Q

_____ predisposes the host to pneumonic pasteurellosis

A

Mycoplasma

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16
Q

Mycoplasma predisposes the host to _______

A

pneumonic pasteurellosis

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17
Q

what is vx against Mannheimia haemolytica based on

A

the 17 serotypes based on capsular suface antigens

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18
Q

Mannheimia haemolytica virulence factors

A

Leukotoxin – induces lysis of leukocytes and platelets
* Capsular polysaccharide (CPS) – prevents phagocytosis
* Lipopolysaccharide (LPS) – Stimulates cytokine releases and microvascular necrosis

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19
Q

Mannheimia haemolytica Pathogenesis

A

Viral infections/environmental stressors lead to shift in the mucosal-commensal
relationship leading to colonization of the organism → Spread to other animals

  • Animals that inhale fomites or infective droplets → bacteria deposit in the mucous layer of the mucociliary apparatus → toxins lead to mucociliary dysfunction → pneumonia
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20
Q

Mannheimia haemolytica lesions

A

Hemorrhagic fibrinonecrotic bronchopneumonia
* Septicemia – fibrinous pleuritis, pericarditis and peritonitis

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21
Q

Histophilus somni etiology

A

Gram-negative, pleomorphic rod
* Fastidious – capnophilic → requires CO2
for growth!

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22
Q

Where does H. somni colonize

A

mucosal surfaces

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23
Q

H. somni pathogenesis

A

Adheres to endothelial cells → induces cytotoxic changes, vasculitis and induction of
apoptosis → formation of fibrinoid thrombi

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24
Q

What are some of the organ systems of cattle affected by H.somni

A

pleuritis +/- bronchopneumonia
myocarditis (causing sudden death)
thrombotic meningoencephalitis
arthritis

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25
Q

H. somni lesions

A

Fibrinous pleuritis, pericarditis, bronchopneumonia
* Focal myocardial lesion
* Polyarthritis
* Fibrinous laryngitis

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26
Q

Mycobacterium bovis etiology

A
  • Very slow-growing, rod-shaped bacteria
  • Weakly Gram-positive – Acid-fast staining
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27
Q

Mycobacterium bovis is a _________ pathogen

A

facultative intracellular pathogen

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28
Q

what populations are reservoirs for Mycobacterium bovis

A

wildlife :
* Bison around Wood Buffalo National Park
* Elk/deer of southwestern Manitoba

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29
Q

Mycobacterium bovis virulence factors

A

Mycosides/phospholipids/sulfolipids – protect against phagocytosis
* Glycolipids – cause a granulomatous response; enhances the survival within phagocytes
* Waxes/tuberculoproteins – induce delayed-type hypersensitivity (tuberculin test)

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30
Q

What does Mycobacterium bovis cause?

A

Bovine TB

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31
Q

Mycobacterium bovis transmission

A

Respiratory secretions & aerosols
* Contaminated milk, feces, urine, vaginal secretions & semen
* Active bovine TB is slow

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32
Q

Mycobacterium bovis clinical signs

A
  • Lethargy, inappetence, emaciation
  • Fluctuating fever and intermittent coughing (dyspnea & tachypnea)
  • Swollen lymph nodes (mediastinal; retropharyngeal)
  • Diarrhea (rare)
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33
Q

Mycobacterium bovis pathogenesis

A

inhalation of aerosols -> infects alveolar macrophages -> proinflammatory cell death -> primary lesion forms -> disemination to secondary sites and lymph nodes -> T cells get primed -> IFNy release from t cells activates macrophages -> macrophages release microbicidal effectors, leading to pulmonary inflammation -> granuloma forms

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34
Q

after a Mycobacterium bovis granuloma forms, what are the three outcomes?

A
  1. Stable granuloma -> latent TB
  2. Stable granuloma -> latent -> reactivation -> active TB
    3.Necrotic granuloma -> active TB
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35
Q

Mycobacterium bovis diagnosis

A
  1. Cell-mediated immune response to intradermal injection of M. bovis antigen
    (Tuberculin test)
  2. In vitro cell-mediated immune test
  3. Culture and PCR testing
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36
Q

T/F Mycobacterium bovis is a reportable disease.

A

true

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37
Q

What is Caudal Fold Tuberculin (CFT)

A

a single intradermal injection of M. bovis to the caudal fold of the tail. After 72 hours, if there is swelling, redness and hardness, the animal is classified as a reactor, and the CFIA must be immediately contacted, with quarantine of the herd.

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38
Q

what is the Comparative Cervical Tuberculin (CCT) test

A

an additional test done on CFT responders. CFIA gives two intradermal injections on the neck within 10 days of infection, then examined after 72 hours. if a reactor, the animal is euthanized and necropsied. if suspected, the animal is retested after 60 days. if negative, yippee!

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39
Q

What are the two intradermal injections given in a CCT

A

M.bocis and M.avium

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40
Q

What happens to any reactor to CFT

A

all infected and potentially in contact animals are quarantined and tested, and a CFIA inspector performs two additional screens (CCT tuberculin and a blood test)

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41
Q

If either the CCT tuberculin or blood test is positive, what happens to the animal

A

it is humanely slaughtered and tissue samples are collected for confirmatory testing (looks for presence of bTB DNA)

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42
Q

If all the adult cattle tests negative to CCT tuberculin and the blood test, what happens

A

the herd is released from quarantine

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43
Q

Which test (CFT or CCT) can a regular vet do

A

CFT. CCT is done by the CFIA

44
Q

in ANY adult cattle test positive to either a blood test or a CCT tuberculin, what happens to the HERD

A

The entire herd (including those which tested negative) will be humanely depopulated, and a new investigation is done to determine potential spread to cows in other herd

45
Q

Mycobacterium bovis lesions

A

Granulomatous lesions of the lungs and mediastinal lymph nodes

46
Q

Mycoplasma spp etiology

A

Very small cell size, highly pleomorphic
* Lack a cell wall
* Slow-growing, fastidious!
* Host-specific!

47
Q

Mycoplasma spp has tropism for

A

specific anatomical sites depending on species → respiratory and/or urogenital

48
Q

How long does culture for M.bovis take?

A

at LEAST 12 weeks

49
Q

Where does Mycoplasma spp attach to

A

ciliated epithelium of trachea, bronchi, bronchioles

50
Q

Mycoplasma spp are ______ pathogens

51
Q

Mycoplasma virulence factors

A

*Adhesins – attachment to host cell surfaces
* Hydrogen peroxide & reactive oxygen species (ROS) – affects ciliary movement
* Biofilm formation – increase resistance to desiccation & heat, impede host defenses
(complement mediated lysis)

52
Q

Mycoplasma pathogenesis

A
  • Adherence to host cells → direct damage to ciliated epithelium → promotes neutrophil and
    mononuclear cellular response → ciliostasis → progresses to pneumonia
53
Q

Mycoplasma lesions

A
  • Bronchitis, bronchiolitis, pneumonia on the Ventral parts of the apical and cardiac lung lobes
  • Pleuropneumonia (Fibrinonecrotic pneumonia, Serofibrinous pleuritis, Serosanguinous fluid in the thoracic cavity)
54
Q

Mycoplasma lesions may become sequestred in a

A

fibrous capsule with viable bacteria

55
Q

Bacterial Respiratory Disease of Sheep and Goats

A

Bibersteinia trehalosi
Mycoplasma ovipneumoniae
+ others

56
Q

Bibersteinia trehalosi etiology

A

Gram-negative, pleomorphic, rods/coccobacilli
* Facultative anaerobe
* Related to Pasteurella (formerly Pasteurella trehalosi

57
Q

Bibersteinia trehalosi is commensial to the

A

tonsils and nasopharynx

58
Q

What is an important opportunistic pathogen of sheep causing bronchopneumonia and septicemia

A

Bibersteinia trehalosi

59
Q

Bibersteinia trehalosi virulence factors

A

same as M.haemolytica:
Leukotoxin
* Capsular polysaccharide
* Lipopolysaccharide

60
Q

Bibersteinia trehalosi pathogenesis

A

Stressors → susceptible to respiratory infections → predisposes to secondary bacterialinfections → once in the lungs (pneumonia) → systemic spread via blood to heart, liver, kidneys, spleen, joints, meninges

61
Q

Bibersteinia trehalosi lesions

A

Fibrinous and ulcerative lesions of the oral cavity – esophagus and larynx

Suppurative bronchopneumonia

Septicemia – myocarditis, hepatitis, nephritis, etc

62
Q

Mycoplasma ovipneumoniae predisposing factors

A

Other bacterial pneumonias (Pasteurellosis) and viral infections
* Stress – weather, crowding, introduction of newly acquired animals

63
Q

Mycoplasma ovipneumoniae clinical signs

A
  • Increased respiratory rates, coughing, nasal discharge, fever, depression of appetite and
    growth rate, drop in milk yields in ewes
64
Q

Mycoplasma ovipneumoniae lesion

A

suppurative bronchopneumonia

65
Q

Bacterial respiratory disease of swine

A

Actinobacillus pleuropneumoniae – APP
Bordetella bronchiseptica (Atrophic rhinitis)

66
Q

Porcine respiratory disease complex = 3 components :

A

primary or secondary bacterial pathogens + Primary or secondary viral pathogens + stressors

67
Q

Actinobacillus pleuropneumoniae – APP etiology

A

Gram-negative coccobacilli
* Fastidious!

68
Q

t/f Actinobacillus pleuropneumoniae (APP) is a relatively unimportant disease

A

FALSE. highly economically damaging disease

69
Q

APP transmission

A

via droplets – requires close contact

70
Q

APP shares a similar disease syndrome to what other bacterial pathogen?

A

Actinobacillus suis

71
Q

APP virulence factors

A
  • Fimbriae – adhesion and attachment
  • Apx toxins – belong within the RTX superfamily of toxins → affinity for alveolar epithelial
    cells, endothelial cells, RBCs, neutrophils and macrophages
  • Proteases – breakdown of host cell proteins
72
Q

APP pathogenesis

A

Close contact exposure → colonization of tonsils and alveolar epithelium →
phagocytosed by macrophages → toxin production → tissue damage (coagulative
necrosis) → severe necrotizing vasculitis → septic shock (peracute death) and/or lung
lesions

73
Q

APP lesions

A
  • Hemorrhagic, fibrinous to necrotizing bronchopneumonia
  • Abscesses and pleuritis
74
Q

Bordetella bronchiseptica etiology

A

Gram-negative coccobacilli
* Obligate aerobe
* Obligate pathogen

75
Q

Bordetella bronchiseptica is a commensal to the

A

upper resp tract of many animals

76
Q

Atrophic rhinitis is a complex disease formed from what two infections>

A

P.multocida (type A or D) and B.bronchiseptica

77
Q

T/F bordetella bronchiseptica is highly contagious

78
Q

B. bronchiseptica virulence factors

A
  • Fimbriae – attachment to host cell respiratory epithelium
  • Adenylate cyclase hemolysin – inhibits phagocytosis
  • Tracheal cytotoxin – damages and paralyzes ciliated tracheal epithelial cells → increase
    mucous secretion, vasoconstriction of blood vessels
  • Dermonecrotic toxin – inhibitory towards osteoblasts
  • LPS – causes influx of neutrophils and macrophages → diphtheric membrane formation
79
Q

Atrophic rhinitis pathogenesis

A

Pre-existing infection with B. bronchiseptica→ colonization and proliferation of P. multocida
→ toxins produced by P. multocida (PM toxin) cause epithelial hypoplasia, atrophy of mucous
glands and osteolysis → dermonecrotic toxin inhibits osteogenesis → atrophy of nasal
turbinates and shrinking of snout

80
Q

Atrophic rhinitis lesions

A
  • Mild, non-progressive lesions
  • Mild to severe turbinate atrophy +/- deviation of the nasal septum
81
Q

Bacterial resp disease of poultry

A

Pasteurella multocida (Fowl Cholera)
Avibacterium paragallinarum (Infectious Coryza)

82
Q

What are the respiratory signs of poultry

A

coughing, rales (crackles), gasping, cyanosis, etc

83
Q

Pasteurella multocida etiology

A

Gram-negative, non-motile rods or coccobacilli
* Facultative anaerobe
* Fastidious

84
Q

What is P.multocida commensal to

A

mucous membranes of oropharynx and GI

85
Q

Pasteurella multocida host range

A

very broad

86
Q

P. multocida virulence factors

A

PM toxin – cytotoxin
* Polysaccharide capsule – prevents phagocytosis, resistance to complement, adherence

87
Q

What does P. multocida cause in birds

A

Fowl cholera

88
Q

Fowl cholera is most common in what species

A

Turkeys (most severe), ducks, geese

89
Q

Fowl cholera is often complicated by:

A

secondary infection

90
Q

Fowl cholera is related to

A

physiological stress

91
Q

What are the two forms of Fowl Cholera

A

Acute: Sudden onset, high morbidity & mortality

Chronic: Survivors of acute form or low virulence strains

92
Q

Acute Fowl Cholera Clinical signs

A

ruffled feathers, depression, increased resp rate, dyspnea, rales, cyanosis

93
Q

Chronic fowl cholera clinical signs

A

assymptomatic or localized exudative infections and inflammation

94
Q

acute Fowl cholera lesions

A

(Septicemia) – hemorrhages, hepatomegaly with focal necrosis, pharyngitis, air
sacculitis, pneumonia, increase pericardial and peritoneal fluids

95
Q

chronic fowl cholera lesions

A

exudative infections (conjunctivitis, sinusitis, otitis media, meningitis), facial
edema (swelling of face, wattles, sternal bursa, legs, joints)

96
Q

Avibacterium paragallinarum etiology

A

Gram-negative, non-motile, small pleomorphic coccobacilli
* Capnophilic – requires CO2
(5-10%)
* Fastidious!
* 3 Serogroups (A, B, C) with 9 serovars

97
Q

What does Avibacterium paragallinarum cause

A

Infectious Coryza

98
Q

T/F Avibacterium paragallinarum has low morbidity but high mortality

A

false. high morbidity and low mortality

99
Q

T/F Avibacterium paragallinarum is highly contagious

100
Q

Avibacterium paragallinarum transmission

A

direct contact, airborne droplets, contaminated drinking water

101
Q

Avibacterium paragallinarum virulence factors

A
  • Capsular polysaccharide (CPS) – mediates attachment to cilia of nasal mucosa
  • Hyaluronic acid – component of capsule → helps to prevent phagocytosis
  • Lipopolysaccharide (LPS) – stimulates inflammatory response
102
Q

what are the two forms of Avibacterium paragallinarum

A

Mild: Young chickens

Severe: Young adults, older birds

103
Q

Mild Infectious coryza clinical signs

A

depression, serous nasal discharge, mild facial swelling in young chickens

104
Q

severe infectious coryza clinical signs

A

depression, diarrhea, decreased feed and water consumption, decreased growth, sneezing, serous/mucoid/suppurative nasal/ocular discharge, facial edema, swollen wattles, rales in adult birds

105
Q

infectious coryza lesions

A

Extreme swelling of infraorbital sinuses with edema
* Sinusitis, conjunctivitis, tracheitis, bronchitis, airsacculitis

106
Q

what is a DDX for infectious coryza

A

P. multocida