Exam 2 Flashcards
Lecture 13-21 (71 cards)
1
Q
Basic life-cycle of a fluke
A
- egg passed in feces that moves through a snail to mature into infectious stage; leaves the snail and infects host.
2
Q
Fasciola hepatica hosts
A
- Definitive: Ruminants, horses, pigs, humans
- Intermediate: Snails
3
Q
Fasciola Hepatica life-cycle
A
- host ingests metacercaria (resistant and infectious stage attached to vegetation) – migrates to liver bile ducts and cases calcified bile ducts and decreased absorption of nutrients.
4
Q
Fasciola Hepatica clinical signs
A
- weakness, anemia, diarrhea, hypoproteinemia
poor production
5
Q
Fasciola Hepatica Diagnosis
A
- fecal sedimentation (too heavy to float)
6
Q
Nanophyetus salmincola hosts
A
- Intermediate: snail and salmon
- Definitive: dogs, cats, bears, raccoons, birds
7
Q
Nanophyetus salmincola pathology
A
- none; it’s a vector for the rickettsial pathogen (Neorickettsia helminthoeca)
8
Q
Salmon poisoning
A
- acute onset symptoms 5-7 days post-infection
- hemorrhagic enteritis caused by Neorickettsia helminthoeca (also dehydration, anorexia, vomiting, diarrhea)
- treat with anti-rickettsial drugs [not anti-helminthics (removal of fluke won’t help)]
9
Q
Nanophyetus salmincola Diagnosis
A
- fecal sedimentation – must treat prior to seeing eggs due to onset of symptoms (5 days) prior to shedding(7 days)
10
Q
Dipylidium caninum
A
- common tapeworm
- flea larvae eats proglottid, it matures in flea, animal will eat flea during grooming and host is infected (small intestine)
11
Q
Taenia spp.
A
- not considered zoonotic
- common in animals that prey on wildlife
- passes an egg in feces rather than a proglottid
- lives in musculature (intermediate host)
12
Q
Taenia solium life-cycle and hosts
A
- definitive host: humans
- intermediate host: pigs or other humans
- lives in porcine musculature until ingested by humans (under-cooked to be infectious); human-human fecal oral contamination possible
13
Q
Taenia saginata
A
- definitive host: humans
- intermediate host: cows or other humans
- lives in bovine musculature until ingested by humans (under-cooked to be infectious); human-human fecal oral contamination possible
- causes cystercercosis (holes in brain)
14
Q
Mesocestoides
A
- common tapeworm of carnivores
- 2 IH (ants and lizards)
- larval tapeworms will fill up the peritoneal cavity (canine peritoneal larval cestoidiasis)
15
Q
Anoplocephala magna
A
- tapeworm in horses
- non-pathogenic unless very heavy load
- ingestion of infected pasture
- IH: mites
16
Q
Moniezia spp.
A
- tapeworm of ruminants
- IH: mites
17
Q
What are the two sub-types of Salmonella of concern as enteric pathogens?
A
- S. enterica,
- S. bongori
18
Q
What are the two types of flagella found on Salmonella?
A
Phase 1 -> common to all enterics
Phase 2 -> unique to salmonella
- only one of these can be expressed at a time
19
Q
3 types of ‘clinical’ salmonella?
A
Host-Restricted: only one host; small infectious dose
Host-Adapted: one main host with potential to infect others; mod. infectious dose
Host-Unrestricted: all species gonna be infected; large infectious dose; most infections stay in GIT
20
Q
Listeria monocytogenes
A
- gram positive rod
- old, young, immunosuppressed
21
Q
L. monocytogenes symptoms
A
- abortion in livestock ruminants
- neuro dz (opisthotonus) , septicemia, liver disease
22
Q
L. monocytogenes virulence mech
A
- adhesion proteins allow for binding to phagocytes
- Listeriolysin O toxin allows escape from phagosome into cytoplasm
- ability to transfer from cell-cell without immune response
23
Q
E. coli (Enterotoxigenic)
A
- Labile toxin - A1B5 toxin causes secretion of Cl- into GI tract –> diarrhea
- Stable toxin - heat resistant; not AB toxin but similar mech ends with diarrhea
- Cytotoxins
- Necrotoxins
considered to be traveller’s diarrhea
fatal in calves <7 days old
24
Q
E. coli (STEC)
A
- O157:H7 – shiga toxin
- AB toxin with B binding to Gb3 (must have this receptor for the toxin to work) (humans have Gb3 on kidneys) (pigs have Gb3 on endothelial cells in brain)
25
E. coli (EPEC)
- physically bind and damage w/ no actual toxin
| - slower cell death than other pathogens
26
Campylobacter spp.
- curved gram negative rod
- microaerophilic
- v small infectious dose
- BAD GI symptoms (bloody diarrhea, cramping)
27
Yersinia spp
- virulence factors affected by temp and [Ca]
| - can survive at lower temps than normally expected
28
Staph. aureus
- dz from ingestion of toxin, not the bacteria
- bacteria killed by cooking, but not the toxin
- acute GI signs (vomiting, cramps, diarrhea)
29
Basic steps in virus infection
1. Attachment (determines specificity/ tropism)
2. Entry (removal of capsid)
3. Uncoating (envelope time)
4. Replication
5. Protein synthesis (ex. capsid proteins)
6. Assembly
7. Release
30
Herpesvirus replication (DNA virus)
1. Attachment normal
2. Entry, Uncoating normal (migration into nucleus)
3. Replication: herpesvirus will encode it's own polymerase to begin replication; early-proteins drive nucleotide replication; late-proteins are for capsid
4. Assembly and Release: envelope gained via budding from nuclear envelope
31
RNA virus site of replication
cytoplasm (DNA is in nucleus)
32
Viral replication and polarity
- positive-sense: the genome itself can be directly transcribed as it reads like mRNA
- negative-sense: RNA carries its own polymerase to create a reverse compliment that will look like mRNA
33
Assembly and Release of enveloped vs non-
enveloped: no need to lyse cell since they are budding
| non-: must lyse cell to escape
34
hemagglutination (HA) vs hemagglutination inhibition (HAI)
HA -- antigen test
| HAI -- antibody test
35
Virus Assay List (virology 2)
EM: presence of virus
qPCR: viral nucleic acids
ELISA, HA: viral antigen
Culture or Plaque: infectivity
36
Giardia spp. hosts
dogs, cats, cattle, horses, humans, etc.
37
Giardia spp. life cycle
- ingestion of cyst (env. resistant stage)
- 2 trophozoites hatch from cyst within SI and begin dividing via binary fission
- trophozoites will encyst prior to excretion
38
Giardia spp. clinical signs
diarrhea
steatorrhea
mucus in stool
weight loss; growth retardation
39
Giardia spp. pathogenesis
stage: trophozoite
mech: ventral adhesive disk interferes with permeability, nutrient uptake, and villus flattening
effects: maldigestion, malabsorptoin, steatorrhea
40
Giardia spp. diagnosis
Direct smear: trophozoite (fresh)
| Flotation: cyst with much easier id
41
Giardia spp. zoonotic potential?
animals to people: rare
| people to people: super common
42
Tritrichomonas foetus description
3 undulating anterior flagella
direct transmission with no cysts
divides via binary fission in warm, moist, anaerobic conditions
43
Tritrichomonas foetus (Bovine)
STD of cattle
Bull: asymptomatic
Cow: Early embryonic death
44
Tritrichomonas foetus (Feline)
resides in distal ileum and colon to cause diarrhea
45
Tritrichomonas foetus diagnosis
- Direct smear
| - PCR (specific and sensitive)
46
Tritrichomonas foetus treatment (Feline)
Usually self-limiting
| metronidazole is ineffective
47
S. Dublin symptoms and host
hosts: cattle
symptoms: cranio-ventral pneumonia, hepatitis, typhiocolitis, diarrhea is less common
48
Clostridium spp. general facts
1. Anaerobic
2. Sporulated
3. Gram positive rods
4. ubiquitous
5. path. involves toxins
49
C. perfringens Type A facts
- Alpha toxin only
- Rarely produce disease (except with Yellow Lamb Disease -- super high alpha toxin levels induce hemolysis)
- Found in everybody
50
C. perfringens Type B facts
- not in the Americas
- Alpha, Beta, Epsilon toxin
- Lamb dysentery
51
C. perfringens Type C facts
- Alpha and beta toxin (necrotizing)
- Beta toxin --> pore forming; very sensitive to trypsin levels (intestinal trypsin is natural defense); Dz predisposed in neonates, pancreatic disease, trypsin inhibitors (colostrum, sweet potato, soybean)
- Enterotoxemia: NEONATES, hemorrhagic diarrhea, neuro signs, sudden death
52
C. perfringens Type D facts
- Alpha and epsilon toxin (neurotoxic)
- Epsilon Toxin --> pore forming, lethal in mice, increases vascular permeability (edema-genic),
- Epsilon Toxin Needs Trypsin Activation
- Clinical signs: neurologic (opisthotonus), resp. difficulty, no diarrhea, focal symmetrical encephalomalacia
53
C. perfringens Type D Goats vs. Sheep
Sheep: Neuro dz
Goats: Neuro or Intestinal lesions or Both
54
C. perfringens Type E Facts
- Alpha and Iota toxin
55
C. perfringens Type F Facts
- Alpha toxin and CPE
- Food poisoning in people
- Diarrhea and abdominal cramps
56
C. perfringens Type G Facts
- Alpha toxin and NetB
- Dz --> Poultry Necrotic Enteritis: massive loss of production and ability of secondary infection to occur
- Diagnosis: must match gross, histo, culture together
57
C. difficile Virulence Factors
- Toxin A: enterotoxin
- Toxin B: cytotoxin, enterotoxin
- CDT
58
C. difficile predisposing factors
1. Antibiotics
| 2. Hospitalization
59
C. difficile clinical lesions/ signs
- diarrhea
- volcano lesions in the large intestine
- piglets get mesocolonic edema
60
C. piliforme fun facts
- only clostridial gram negative
| - Triad of Lesions: hepatitis, colitis, myocarditis
61
Black Leg in Cattle (etiology, pathogenesis)
Etiology: C. Chauvoei
Pathogenesis: ingested and migration to musculature where they are picked up by macrophages and sequestered; trauma --> decreased O2 --> germination, replication, and toxin production
62
Gas Gangrene (etiology, pathogenesis)
Etiology: human = C. perfringens; Animals = multiple species
Pathogenesis: laceration wound allows bacteria to enter and infect; low O2 environment allows for proliferation; germination and toxin production
(normally affects SQ as doesn't go systemic)
63
Hepatitis from a clostridia (etiology and types, pathogenesis)
Etiology: C. novyi
Type A (gas gangrene in animals and humans)
Type B (necrotic hepatitis in sheep)
Type D (bovine bacillary hemoglobinuria)
Pathogenesis: black leg but hepatic macrophages
Predisposing factors: Fasciola hepatica
64
Eimeria spp. (host specificity and life-cycle)
- very host specific (non-zoonotic)
- Life-cycle: excrete unsporulated oocyst --> sporulated oocyst with 4 sporocysts --> each sporocyst has 2 sporozoites
- Asexual and Sexual reproduction
65
Eimeria spp. (pathogenesis)
- damage from asexual and sexual reproduction as they damage enterocytes
- degree of damage/ infection depends on host immune status, infective dose, etc
66
Eimeria spp. (diagnosis)
- fecal flotation for oocyst (look at size)
67
Cryptosporidium spp. (host specificity and life-cycle)
- not host specific
- Life-cycle: found in feces is a sporulated oocyst (directly infectious via fecal-oral contamination); invasion into enterocyte brush border for reproduction (less chance for hem. diarrhea than Eimeria)
68
Cryptosporidium spp. (-osis and Diagnosis and Control)
- -osis: self-limiting, small bowel diarrhea
- Diagnosis: zinc sulfate flotation, Acid fast stain
- Control: most serious clinical dz in calves; no treatment
69
Cystoisospera (species infected)
- puppies, kittens, piglets
| - v. host specific (non-zoonotic)
70
Cystoisospera (Life-cycle)
- Excrete unsporulated oocyst --> sporulated oocyst with 2 sporocysts --> each sporocyst has 2 sporozoites
- possibility for paratinic hosts
71
Cystoisospera (symptoms, predisposition, diagnosis)
- Symptoms: diarrhea, weight loss, dehydration, rarely hemorrhage
- Predisposition: immunocompromised, young, stressed
- Diagnosis: proof of oocysts in feces does not mean infectious/ that is the disease
