Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRH II > Blood Borne Infections- SA > Flashcards

Blood Borne Infections- SA Flashcards

1
Q

describe ehrlichiosis type and mode of transmission

A
  1. 3 species:
    -E. canis, ewingii, chaffeensis
    -intracellular gram negative bacteria
    -E. canis causes canine monocytic ehrlichiosis, worldwide distribution
    -ewingii and chaffeensis southern USA, africa
    -within family anaplasmataceae
  2. mode of transmission:
    -tickborne
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe ehrlichiosis clinical signs

A

Major clinical signs:

-E. canis: fever, lethargy, inappetance, wt loss, cutaneous/mucosal petechia/ecchymotic hemorrhages!!!, lymphadenomegaly, splenomegaly, uveitis
–cats: fever, lethargy, inappetance, weight loss, hyperesthesia, joint patin

E. ewingii: fever, lethargy, inappetance, polyarthritis

CAN infect and cause disease in humans!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe cytologic characteristics of ehrlichiosis

A

form morulae (the organisms themselves) within phagosomes of circulating leukocytes

E. canis: monocytes and macrophages,&raquo_space;lymphocytes
-canine monocytic ehrlichiosis

E. ewingii: granulocytes
-canine granulocytic ehrlichiosis

E. chaffeensis: human monocytic ehrlichiosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe canine monocytic ehrlichiosis as caused by E. canis

A
  1. acute, subclinical, and chronic phases
  2. thombocytopenia most commonly seen (1-4 weeks post infection) in >90% of acute infections; usually mild to moderate
    -likes to replicate in reticuloendothelial tissue = lymphadenomegaly and splenomegaly
  3. +/- morulae within circulating monocytes in acute infection
  4. chronic and severe can result in severe monoclonal gammopathy (not neoplastic) (FYI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe E. canis diagnosis

A
  1. serology:
    -IFA: gold standard, but abs only detected 7-28d post infection, so false negative common with acute infection!

-ELISA: (SNAP 4DX)- antibodies, so also false negative with acute; does not distinguish between types of ehrlichia

-western immunoblotting (research primarily)

  1. PCR: whole blood, helpful for acute infection
  2. ideal: serology + PCR
    -positive serum Ab titer may reflect PREVIOUS exposure vs active infection, so retest 2-3 weeks later and interpret in light of clinical signs!

-high titers do NOT correlate with severity of hyperglobulinemia, disease, or duration of illness

-cross reactivity with E, chaffeensis > E. eqingii, A. phagocytophilum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe E. canis treatment

A
  1. supportive care
  2. antibiotics!
    -doxycycline: high blood, tissue, and IC concentration
    -dose: don’t actually know best dose or duration, base on clinical signs and recovery
  3. clinical improvement should be within 24-48 hours
    -platelets within ref range within 10-14d post starting treatment
  4. dogs can be reinfected!
    -titers decline and become negative within 6-9 months post treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe E. chaffeensis

A
  1. experimentally infected dogs: fever, thrombocytopenia, leukopenia
  2. possible persistent carrier state in dogs (bone marrow, spleen, liver, LN, lungs, kidneys, brain)
    -white-tailed deer may also be reservoir hosts in north america
  3. diagnosis:
    -serology: detectable ab titers 7-23d post infection, cross reactivity with other ehrlichia spp.
    -RT-PCR
  4. treatment: abx: doxycycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe E. ewingii

A
  1. infected dogs can serve as a reservoir host
    -replicates in neutrophils, usually subclinical
  2. acute disease (2-3 weeks post infection): fever, lethargy, anorexia, lameness (neutrophilic polyarthritis), possible neurologic manifestations
  3. diagnosis:
    -morulae prior to serconversion or clin signs
    -thrombocytopenia (43%), anemia, mild to moderate neutrophilic leukocytosis with left shift
    -serology: abs present approx 1 month post inoculation
    –ELISA: cross reacts with other ehrlichia spp.
    –false negative with acute illness
    -PCR: positive as early as 4 days post inoculation
  4. treatment: doxycycline
    -rapid clinical improvement within 24-48 hr
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe anaplasmosis

A
  1. 2 species:
    -anaplasma platys: canine thrombocytotropic anaplasmosis
    -anaplasma phagocytophilum: canine granulocytic anaplasmosis
  2. obligate intracellular gram negative pleomorphic bacteria
    -obligate aerobes
    -lack cell wall
  3. geographic distribution:
    -A. platys: throughout Americas
    -A. phagocytophilum: upper midwestern, northeastern, western states
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe anaplasmosis transmission

A

tick borne!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe major clinical signs of anaplasmosis

A
  1. A. platys: maybe fever, lethargy
  2. A. phagocytophilum: fever, lethargy, inappetance, lameness (polyarthritis)
  3. causes human granulocytic anaplasmosis (A. phagocytophilum)
    -dogs = sentinels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe anaplasma phagocytophilum/canine granulocytic anaplasmosis

A
  1. tropic for granulocytes (esp neutrophils): forms morulae within them
  2. tick must be attached 24-48 hours for transmission to occur (prevention is key!)
  3. mild to moderate, occasionally severe thrombocytopenia (approx 90%)
    - +/- other cytopenias
  4. self-limiting in many infected dogs and cats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe diagnosis and treatment of anaplasma phagocytophilum/canine granulocytic anaplasmosis

A

diagnosis:
1. morulae within granulocytes as early as 4 days post inoculation

  1. acute and convalescent serology (titers)/ELISA for antibodies
  2. PCR for acute infection without morulae

treatment:
1. doxycycline!
-clinical improvement within 24-48 hrs of tx
-platelet counts normalize within 2-14d of treatment initiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe anaplasmosis platys/infectious canine cyclic thrombcytopenia (ICCT)

A
  1. platelet tropism
    -thrombocytopenia +/- mild, nonregenerative anemia
    -cycles of thrombocytopenia every 1-2 weeks
  2. diagnosis:
    -morulae in platelets 7-19d post infection
    -serology: cross reacts with other anaplasma spp
    –ELISA: false negative in acute infection
    –paired titers
    -PCR
  3. treatment: doxycycline!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe rickettsia rickettsii

A
  1. AKA rocky mountain spotted fever
    -gram negative obligate IC bacteria
    -infect endothelial cells!!!!
    -affects humans and dogs
    -part of family rickettsiaceae
  2. major clinical signs:
    -acute febrile illness
    -vasculitis
    -vomiting
    -ocular signs (retinal hemorrhage, uveitis, episcleral injection)
    -lymphadenomegaly
    -splenomegaly
    -peripheral edema
    -cutaneous hyperemia and necrosis
    -polyarthritis
    -neurologic signs
  3. geographic distribution: north, central, south america (ALL of US)
  4. most of transmission: ticks, everywhere!
    -can also spread cell to cell without rupturing the cell = immune system evasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe clinical presentation of rickettsia rickettsii

A
  1. young and purebred dogs potentially overrepresented
    -english springer spaniels with phosphpfructokinase deficiency
    -GSDs
  2. endotheliotropic = disseminated vasculitis
    -spreads through lymphatics or directly into bloodstream to small capillaries
    -primarily infects endothelial cells, smooth muscles and monocytes can be infected though
  3. primarily an acute disease!
    -thrombocytopenia common (vasculitis and immune-mediated platelet destruction)
    -get bit get sick quick
  4. diagnosis:
    -acute CS + PCR or IHC = active infection

-seroconversion: positive titer only indicates exposure; acute and convalescent titers needed (4-fold change to confirm infection)

-PCR: especially in acute phase: false negatives due to low numbers of organisms, transient circulation, or abx therapy

  1. treatment:
    -should be started before confirmed diagnosis
    -doxycycline! 7 days usually adequate
    -rapid clinical response (24-48hr)

-possible lifelong immunity to reinfection

17
Q

describe cytauxzoonosis

A
  1. cytauxzoon felis
    -hematoprotozoal parasite
  2. two distinct forms:
    –nonerythrocytic: schizont
    –erythrocytic: piroplasm
  3. bobcat = reservoir host
    -arthropod vectors: tick borne
  4. geographic distribution: midwest, south central, southeastern, mid-atlantic states; expanded with expansion of A. anericanum range
    -outdoor cats in spring and summer, more prevalent in rural and suburban areas (prevention is key!!)
  5. transmission: feeding of vector ticks
    -no human health significance
18
Q

describe cytauxzoonosis clinical presentation

A
  1. clinical disease: 1-3 weeks after infection
    -rapid clinical course: death within days
  2. major clinical signs:
    -rapidly progressive febrile illness (up to 107F)
    -icterus
    -pallor
    -lymphadenomegaly
    -splenomegaly: should NOT be able to feel cat spleen
    -hepatomegaly
    -seizures
    -could be subclinical, but if symptomatic = most likely dead soon
19
Q

describe diagnosis of cytauxzoonosis

A
  1. ID RBC parasites on blood smear!
    -piroplasms shaped as signet rings within RBCs
    -distinguish from M. hameofelis: epicellular cocci/rods/rings
  2. PCR: may remain positive in recovered cats
  3. cytology:
    -schizonts within mononuclear cells
    -schizont-laden macrophages on FNA (LN, spleen, liver)

serology not mentioned bc some animals die before the body has a chance to make Abs :(

20
Q

describe treatment of cytauxzoonosis

A
  1. supportive intensive care
    -IVF
    -RBC transfusion for severe anemia
    –heparin for clot formation associated with DIC but CAREFUL if already bleeding
  2. antiprotozoal therapy:
    -imidocarb: may lack efficacy (26% survival rate)
    -atovaquone and azithromycin: improved survival rate compare to imidocarb (60% survival rate)
  3. no vaccine, preventing tick bite is key!!
21
Q

describe hemotropic mycoplasms

A
  1. gram neg, obligate epierythrocytic bacteria, wall-less, non-acid fast, not culturable!
    -formerly haemobartonella and epierythrozoon
  2. includes:
    -dogs: M. haemocanis, candidatus mycoplasma haemotoparvum

cats: M. haemofelis, candidatus mycoplasma haemominitum, candidatus mycoplasma turicensis

  1. geographic distribution: worldwide
22
Q

describe mode of transmission, major clinical signs, and zoonotic capability of hemotropic mycoplasms

A

modes of transmission:
1. tickborne
2. other arthropods: fleas, mosquitoes
3. biting/aggressive interactions
4. vertical transmission
5. ingestion/injection of infected blood (blood transfusions)

major clinical signs:
-fever, lethargy, inappetance, weakness, pallor, dehydration

possible zoonotic infections (potentially)

23
Q

describe hemotropic mycoplasmas in cats

A
  1. M. haemofelis
    -candidatus mycoplasma haemominutum
    -candidatus mycoplasma turicensis
    (candidatus = new and incompletely described)
  2. blood film: small, dark blue-staining rods, cocci, or slightly larger ring forms
    -Candidatus M. haemominutum- rarely seen in blood films (tiny)

-may see loss of normal RBC appearance and shape

  1. exact prevalence difficult to determine
  2. clinical disease most associated with M. haemofelis: severe hemolytic anemia, macrocytic, hypochromic, regenerative (but pronounced reticulocytosis not always evident)
    -positive Coombs (esp cold agglutinins); autoagglutination in the acute phase
    -FIV/FeLV positive (predisposes)
24
Q

describe M. haemofelis

A
  1. clinical signs within 2-34 days post infection
  2. anemia lasting 18-30 days
  3. M. haemofelis blood organism numbers fluctuate greatly
  4. chronic infection not usually associated with significant anemia
25
Q

describe candidatus M. haemominutum

A
  1. no clinical illness or significant anemia
    -carrier status common
  2. occasional reports of only recognizable cause of anemia in some naturally infected cats (co-infection usually required)
  3. risk factoes:
    -older age
    -outdoor exposure
    -cutaneous SCC
    -stomatitis
    -FIV and/or FeLV +

plus C. M. tericensis: moderate to severe hemolytic anemia

26
Q

describe hemotropic mycoplasmas in dogs (M. haemocanis)

A
  1. experimental transmission via tick
  2. blood transfusions can cause infection
  3. prepatent period: 1-2d to 2+ weeks
    -some with rapidly progressive anemia and death within approx 1 month post infection
    -sone with gradual anemia with repetitive parasitemic episodes
  4. hemolytic anemia: +/- positive coomb’s test
  5. approx 1-2 months required fr HCT to drop to minimum and 1-2 months to recovery
  6. splenectomy in dogs almost always required for dogs to become clinical!
  7. more commonyl forms chains on surface of RBCs, can see small cocci, rods, rings
  8. candidatus mycoplasma haematoparvum: novel, small hemoplasma
27
Q

describe diagnosis of hemotropic mycoplasma

A
  1. direct cytologic exam
    -stained blood smears: approx 50% accurate in the acute phase
  2. PCR based assays: highly sensitive
    -can have subclinical carrier state
    -interpret positive results in light of clinical signs
  3. culture is unsuccessful!
28
Q

describe therapy and prevention of hemotropic mycoplasmas

A
  1. supportive care
  2. antimicrobial therapy:
    -does not predictably clear organism from body!!
    -doxycycline, marbofloxacin, pradofloxacin and enrofloxacin are second line drugs
  3. clinical improvement within 2-3 days of starting treatment
  4. prevention!
    -flea/tick preventative
    -screen blood donors (PCR preferred)
29
Q

describe canine babesiosis

A
  1. intraerythrocytic protozoan parasite
  2. many species
  3. geo distrib: worldwide
  4. major clin signs:
    -lethargy, pallor, splenomegaly, subclinical
    -no human health concerns
30
Q

describe babesiosis transmission

A
  1. B. canis (vogeli): brown dog tick, most common in southern US, greyhounds!!!
  2. B. gibsoni:
    -NON VECTOR transmission most common: dog fighting wounds!!!!
    -or transplacental
31
Q

describe babesia in greyhouds and APBTs

A

greyhounds: B. canis
-reported rates of positive carriers: 20-60%
-risk considered low for clinical disease, but increases in a kennel situation
-IMPORTANT: know the seropositive status of adopted greyhounds

pit bull terriers: B. gibsoni
-most cases reported in US in this breed
-if another dog breed is positive for B. gibsoni, important to ask if they’ve been in a fight with an APBT- history is important!

32
Q

describe pathogenesis of canine babesiosis

A
  1. infected RBCs have parasite antigens on their surface, inducing host-opsonizing antibodies to remove infected erythrocytes via mono-nuclear phagocyte system
  2. hosts develop anti-RBC membrane antibodies against self antigens, resulting in immune-mediated anemia
  3. thrombocytopenia occurs due to consumption of platelets +/- immune-mediated
  4. HEMOLYTIC ANEMIA and THROMBOCYTOPENIA
    -anemia initially mild, normocytic, normochromic
    -then macrocytic, hypochromic, and regenerative
  5. a splenectomy makes the parasitemia and anemia more severe
33
Q

describe diagnosis of babesiosis

A
  1. microscopic identification:
    -large spp. 3-5 um in length: B. canis, vogeli, rossi
    -small spp. 1-3 um in length: B. gibsoni, conradae, vulpes
  2. serologic testing:
    -IFA
    -convalescent titers
  3. nucleic acid-based detection
    -PCR: required for accurate species ID
  4. parasite visualization:
    -capillary blood: ear tip or nail bed
    -negative slide exam does not rule it out! poor sensitivity
  5. there is NO perfect test!
34
Q

describe treatment of babesiosis

A
  1. imidocarb diproprionate
    -side effects: pain, autonomic signs
    -likely curative for B. canis, vogeli, rossi
    -reduces morbidity and mortality for B. gibsoni: does NOT cure!
  2. atovaquone and azithromycin combination therapy
    -more effective treatment for B. gibsoni, conradae
    -use liquid suspension of atovaquone
  3. clindamycin, metronidazole, and doxocycline combination therapy
    -for B. gibsoni if fail atovaquone/azithromycin for a minimum of 3 months, with uncertain efficacy
35
Q

describe tularemia

A
  1. francisella tularensis: gram negative coccobacillus, facultatis intracellular bacteria, aerobia
  2. mode of transmission: inoculation, skin/mucosal contact, aerosol inhalation, ingestions, vector transmission
  3. major vectors:
    -ticks
    -biting flies
  4. geographic distribution: norther hemisphere, virulent strains prevalent in USA
  5. major clinical signs: fever, lethargy, lymphadenopathy, SC abscesses, splenomegaly, hepatomegaly, GI
  6. young adult cats and dogs; cats more susceptible
  7. DO NOT CULTURE; REPORTABLE; WILL INFECT HUMAN

CRH II (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions