Respiratory pathogens 1 (tesse) Flashcards
1
Q
Where is the ciliated epithelium in the resp tract
A
nasal epithelium
bronchi
trachea
pharynx (?)
2
Q
what is the function of the ciliated epithelium
A
muco-ciliary apparatus
3
Q
What are the three bacteria with tropism for the ciliated epithelium
A
Bordetella
Mycoplasma
Chlamydia
4
Q
What are the three routes of infection into the respiratory tract
A
aerosol
particle/droplet
conjuctival
5
Q
what determines the severity, type and location of respiratory infection
A
bacterial virulence factors
6
Q
what are the types of respiratory infections
A
pharyngitis/laryngitis
tracheitis
bronchitis
pneumonia
etc
7
Q
what virulence factors are responsible for Adherence and resistance to expulsion:
A
- Pili (Fimbriae)
- Adhesins
- Biofilm
8
Q
what virulence factors are responsible for Survival in infected cells:
A
- Ability to compete for iron
- Survival in phagosomes
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
10
Q
what virulence factors are responsible for Disease production/damage host:
A
- Super antigens
- Cell wall components
11
Q
What are the main resp pathogens of cattle
A
Mannheimia haemolytica
Pasteurella multocida
Bibersteinia trehalosi
Histophilus somni
Mycoplasma bovis
Mycobacterium bovis
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)
13
Q
etiology of Mannheimia haemolytica
A
- Gram-negative, pleomorphic rod/coccobacilli
- Related to Pasteurella (formerly Pasteurella haemolytica)
- Fastidious
14
Q
Mannheimia haemolytica is commensal to the
A
oropharynx
15
Q
_____ predisposes the host to pneumonic pasteurellosis
A
Mycoplasma
16
Q
Mycoplasma predisposes the host to _______
A
pneumonic pasteurellosis
17
Q
what is vx against Mannheimia haemolytica based on
A
the 17 serotypes based on capsular suface antigens
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
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
20
Q
Mannheimia haemolytica lesions
A
Hemorrhagic fibrinonecrotic bronchopneumonia
* Septicemia – fibrinous pleuritis, pericarditis and peritonitis
21
Q
Histophilus somni etiology
A
Gram-negative, pleomorphic rod
* Fastidious – capnophilic → requires CO2
for growth!
22
Q
Where does H. somni colonize
A
mucosal surfaces
23
Q
H. somni pathogenesis
A
Adheres to endothelial cells → induces cytotoxic changes, vasculitis and induction of
apoptosis → formation of fibrinoid thrombi
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
25
H. somni lesions
Fibrinous pleuritis, pericarditis, bronchopneumonia
* Focal myocardial lesion
* Polyarthritis
* Fibrinous laryngitis
26
Mycobacterium bovis etiology
* Very slow-growing, rod-shaped bacteria
* Weakly Gram-positive – Acid-fast staining
27
Mycobacterium bovis is a _________ pathogen
facultative intracellular pathogen
28
what populations are reservoirs for Mycobacterium bovis
wildlife :
* Bison around Wood Buffalo National Park
* Elk/deer of southwestern Manitoba
29
Mycobacterium bovis virulence factors
Mycosides/phospholipids/sulfolipids – protect against phagocytosis
* Glycolipids – cause a granulomatous response; enhances the survival within phagocytes
* Waxes/tuberculoproteins – induce delayed-type hypersensitivity (tuberculin test)
30
What does Mycobacterium bovis cause?
Bovine TB
31
Mycobacterium bovis transmission
Respiratory secretions & aerosols
* Contaminated milk, feces, urine, vaginal secretions & semen
* Active bovine TB is slow
32
Mycobacterium bovis clinical signs
* Lethargy, inappetence, emaciation
* Fluctuating fever and intermittent coughing (dyspnea & tachypnea)
* Swollen lymph nodes (mediastinal; retropharyngeal)
* Diarrhea (rare)
33
Mycobacterium bovis pathogenesis
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
34
after a Mycobacterium bovis granuloma forms, what are the three outcomes?
1. Stable granuloma -> latent TB
2. Stable granuloma -> latent -> reactivation -> active TB
3.Necrotic granuloma -> active TB
35
Mycobacterium bovis diagnosis
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
36
T/F Mycobacterium bovis is a reportable disease.
true
37
What is Caudal Fold Tuberculin (CFT)
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.
38
what is the Comparative Cervical Tuberculin (CCT) test
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!
39
What are the two intradermal injections given in a CCT
M.bocis and M.avium
40
What happens to any reactor to CFT
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)
41
If either the CCT tuberculin or blood test is positive, what happens to the animal
it is humanely slaughtered and tissue samples are collected for confirmatory testing (looks for presence of bTB DNA)
42
If all the adult cattle tests negative to CCT tuberculin and the blood test, what happens
the herd is released from quarantine
43
Which test (CFT or CCT) can a regular vet do
CFT. CCT is done by the CFIA
44
in ANY adult cattle test positive to either a blood test or a CCT tuberculin, what happens to the HERD
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
Mycobacterium bovis lesions
Granulomatous lesions of the lungs and mediastinal lymph nodes
46
Mycoplasma spp etiology
Very small cell size, highly pleomorphic
* Lack a cell wall
* Slow-growing, fastidious!
* Host-specific!
47
Mycoplasma spp has tropism for
specific anatomical sites depending on species → respiratory and/or urogenital
48
How long does culture for M.bovis take?
at LEAST 12 weeks
49
Where does Mycoplasma spp attach to
ciliated epithelium of trachea, bronchi, bronchioles
50
Mycoplasma spp are ______ pathogens
obligate
51
Mycoplasma virulence factors
*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
Mycoplasma pathogenesis
* Adherence to host cells → direct damage to ciliated epithelium → promotes neutrophil and
mononuclear cellular response → ciliostasis → progresses to pneumonia
53
Mycoplasma lesions
* 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
Mycoplasma lesions may become sequestred in a
fibrous capsule with viable bacteria
55
Bacterial Respiratory Disease of Sheep and Goats
Bibersteinia trehalosi
Mycoplasma ovipneumoniae
+ others
56
Bibersteinia trehalosi etiology
Gram-negative, pleomorphic, rods/coccobacilli
* Facultative anaerobe
* Related to Pasteurella (formerly Pasteurella trehalosi
57
Bibersteinia trehalosi is commensial to the
tonsils and nasopharynx
58
What is an important opportunistic pathogen of sheep causing bronchopneumonia and septicemia
Bibersteinia trehalosi
59
Bibersteinia trehalosi virulence factors
same as M.haemolytica:
Leukotoxin
* Capsular polysaccharide
* Lipopolysaccharide
60
Bibersteinia trehalosi pathogenesis
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
Bibersteinia trehalosi lesions
Fibrinous and ulcerative lesions of the oral cavity – esophagus and larynx
Suppurative bronchopneumonia
Septicemia – myocarditis, hepatitis, nephritis, etc
62
Mycoplasma ovipneumoniae predisposing factors
Other bacterial pneumonias (Pasteurellosis) and viral infections
* Stress – weather, crowding, introduction of newly acquired animals
63
Mycoplasma ovipneumoniae clinical signs
* Increased respiratory rates, coughing, nasal discharge, fever, depression of appetite and
growth rate, drop in milk yields in ewes
64
Mycoplasma ovipneumoniae lesion
suppurative bronchopneumonia
65
Bacterial respiratory disease of swine
Actinobacillus pleuropneumoniae – APP
Bordetella bronchiseptica (Atrophic rhinitis)
66
Porcine respiratory disease complex = 3 components :
primary or secondary bacterial pathogens + Primary or secondary viral pathogens + stressors
67
Actinobacillus pleuropneumoniae – APP etiology
Gram-negative coccobacilli
* Fastidious!
68
t/f Actinobacillus pleuropneumoniae (APP) is a relatively unimportant disease
FALSE. highly economically damaging disease
69
APP transmission
via droplets – requires close contact
70
APP shares a similar disease syndrome to what other bacterial pathogen?
Actinobacillus suis
71
APP virulence factors
* 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
APP pathogenesis
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
APP lesions
* Hemorrhagic, fibrinous to necrotizing bronchopneumonia
* Abscesses and pleuritis
74
Bordetella bronchiseptica etiology
Gram-negative coccobacilli
* Obligate aerobe
* Obligate pathogen
75
Bordetella bronchiseptica is a commensal to the
upper resp tract of many animals
76
Atrophic rhinitis is a complex disease formed from what two infections>
P.multocida (type A or D) and B.bronchiseptica
77
T/F bordetella bronchiseptica is highly contagious
true
78
B. bronchiseptica virulence factors
* 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
Atrophic rhinitis pathogenesis
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
Atrophic rhinitis lesions
* Mild, non-progressive lesions
* Mild to severe turbinate atrophy +/- deviation of the nasal septum
81
Bacterial resp disease of poultry
Pasteurella multocida (Fowl Cholera)
Avibacterium paragallinarum (Infectious Coryza)
82
What are the respiratory signs of poultry
coughing, rales (crackles), gasping, cyanosis, etc
83
Pasteurella multocida etiology
Gram-negative, non-motile rods or coccobacilli
* Facultative anaerobe
* Fastidious
84
What is P.multocida commensal to
mucous membranes of oropharynx and GI
85
Pasteurella multocida host range
very broad
86
P. multocida virulence factors
PM toxin – cytotoxin
* Polysaccharide capsule – prevents phagocytosis, resistance to complement, adherence
87
What does P. multocida cause in birds
Fowl cholera
88
Fowl cholera is most common in what species
Turkeys (most severe), ducks, geese
89
Fowl cholera is often complicated by:
secondary infection
90
Fowl cholera is related to
physiological stress
91
What are the two forms of Fowl Cholera
Acute: Sudden onset, high morbidity & mortality
Chronic: Survivors of acute form or low virulence strains
92
Acute Fowl Cholera Clinical signs
ruffled feathers, depression, increased resp rate, dyspnea, rales, cyanosis
93
Chronic fowl cholera clinical signs
assymptomatic or localized exudative infections and inflammation
94
acute Fowl cholera lesions
(Septicemia) – hemorrhages, hepatomegaly with focal necrosis, pharyngitis, air
sacculitis, pneumonia, increase pericardial and peritoneal fluids
95
chronic fowl cholera lesions
exudative infections (conjunctivitis, sinusitis, otitis media, meningitis), facial
edema (swelling of face, wattles, sternal bursa, legs, joints)
96
Avibacterium paragallinarum etiology
Gram-negative, non-motile, small pleomorphic coccobacilli
* Capnophilic – requires CO2
(5-10%)
* Fastidious!
* 3 Serogroups (A, B, C) with 9 serovars
97
What does Avibacterium paragallinarum cause
Infectious Coryza
98
T/F Avibacterium paragallinarum has low morbidity but high mortality
false. high morbidity and low mortality
99
T/F Avibacterium paragallinarum is highly contagious
true
100
Avibacterium paragallinarum transmission
direct contact, airborne droplets, contaminated drinking water
101
Avibacterium paragallinarum virulence factors
* 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
what are the two forms of Avibacterium paragallinarum
Mild: Young chickens
Severe: Young adults, older birds
103
Mild Infectious coryza clinical signs
depression, serous nasal discharge, mild facial swelling in young chickens
104
severe infectious coryza clinical signs
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
infectious coryza lesions
Extreme swelling of infraorbital sinuses with edema
* Sinusitis, conjunctivitis, tracheitis, bronchitis, airsacculitis
106
what is a DDX for infectious coryza
P. multocida
107
