Term
|
Definition
Platyhelminthes; Trematoda; Digenea
Somewhat leaf-shaped
Incomplete digestive systems
Blind sac with two cecae
Hermaphroditic (except schistosomes)
One ovary and two testes
Suckers present |
|
|
Term
|
Definition
Adults in vertebrates
First intermediate host is a snail
Asexual reproduction occurs in snail
May or may not use second intermediate host depending on species
No asexual reproduction in these additional hosts |
|
|
Term
| Name 3 important flukes of companion animals |
|
Definition
Platynosomum concinnum - Liver fluke of Cats
Paragonimus kellicotti - Lung fluke of Cats & Dogs
Nanophyetus salmincola - Salmon poisoning fluke of Cats & Dogs
All are accidental infections from sylvatic life cycles normally involving various wildlife |
|
|
Term
|
Definition
Platynosomum concinnum
Lives in the bile ducts and gall bladder of felids and skunks
Most common liver fluke of cats in North America
Not very common & seen mainly in tropical/subtropical climates
Found in the coastal southeast (especially Florida), the Caribbean and Pacific Islands |
|
|
Term
| Platynosomum consimmum Life Cycle |
|
Definition
The first IH is a terrestrial snail
Only sporocysts develop, no redial stage
May use pillbugs as a paratenic host
Cats are infected by hunting and eating second intermediate hosts - some lizards and frogs
Contain mesocercariae (resting but non-encysted cercariae)
Enter common bile duct & mature
Prepatent period 8 weeks |
|
|
Term
| Signs of Platynosomum Consinnum infection? |
|
Definition
Most infections asymptomatic
Clinical signs appear with heavy infections
Non specific
Weight loss, vomiting, diarrhea, abdominal distension, hepatomegaly, depression, anorexia & icterus accompanied by eosinophilia |
|
|
Term
| Pathology of Platynosomum concinnum (liver fluke)? |
|
Definition
“Lizard poisoning” of cats
Icterus due to biliary obstruction
Hepatomegaly with fibrosis of bile ducts, epithelial hyperplasia
Cirrhosis of liver
Diarrhea & vomiting |
|
|
Term
| How can we diagnose feline liver fluke (Platynosomum Concinnum)? |
|
Definition
Diagnosis
Sedimentation of feces
Tiny eggs about 35 - 40 microns in length, with indistinct operculum, often dark brown
Adults seen in histologic sections and at necropsy
Appropriate clinical signs in endemic areas
May demonstrate enlarged bile ducts & even flukes with ultrasound |
|
|
Term
| Treatment of liver flukes? Platynosomum concinnum? |
|
Definition
Treatment
Old protocol was surgical removal
Praziquantel most effective
Each practice seems to have its own protocol established empirically
should be at least 20 mg/kg dose
some use it daily for 3 or 5 days, others every other day for some duration
Nothing is proven by controlled clinical trial
Epsiprantel & fenbendazole reported to have some efficacy |
|
|
Term
| How to preven liver flikes? |
|
Definition
Keep cats indoors to prevent hunting
Praziquantel every 3 months has been suggested for cats at high risk |
|
|
Term
|
Definition
Adults are parasites of mink, muskrat, raccoon and fox reservoir hosts
Dogs & cats are accidentally infected
Adults found (usually in pairs) in cysts in the lung parenchyma
Primarily in the Great Lakes region, but also occur in isolated foci in the southeast, including the Florida panhandle |
|
|
Term
| Paragonimus kellicotti life cycle? |
|
Definition
Life Cycle
Eggs shed in feces hatch and the miracidia penetrate an aquatic snail
Sporocysts & rediae develop in the snail
Snails shed cercariae that encyst as metacercariae in crayfish
Dogs and cats are infected by preying on crayfish in fresh water habitats
Juvenile flukes enter the peritoneal cavity by penetrating the intestinal wall
Wander in the peritoneal cavity for up to 2 weeks
Penetrate the diaphragm & pleural surface of the lungs and encyst in the parenchyma
Prepatent period is 2-7 weeks |
|
|
Term
| Paragonimus kellicotti pathology? |
|
Definition
Pathology
Signs chronic coughing, hemopsis, pneumonia
Atelectasis (collapse of alveoli)
Pneumothorax if cyst ruptures |
|
|
Term
| Diagnosis of Paragonimus kellicotti? |
|
Definition
Diagnosis
Fecal sedimentation and finding eggs with very distinct operculum and measuring 80 - 95 microns in length
Appropriate clinical signs in endemic area
Be highly suspicious of Paragonimus in cases of unexplained pneumothorax within endemic areas.
Remember the snow birds |
|
|
Term
| Treatment and control of Paragonimus kellicotti |
|
Definition
Treatment and Control
Praziquantel 25 mg.kg t.i.d. for 2-3 days
Fenbendazole 50 mg/kg b.i.d. for 5 days or s.i.d. for 10-14 days
Prevent cats and dogs from hunting along freshwater habitats |
|
|
Term
|
Definition
Salmon poisoning fluke of dogs
Infects canids, felids, bears, and other fish eating small mammals
Occurs in the Northwestern U.S., especially west of the Cascades
Tiny fluke - about 1.5 mm: Name means “grow to be a dwarf and live in salmon”. |
|
|
Term
| Life cycle of Nanophyetus salmincola? |
|
Definition
Eggs shed in feces, hatch and miracidia penetrate a snail
A single snail species that inhabits small streams
Develops directly to rediae, which shed cercariae
No sporocyst stage
Cercariae infect trout and salmon, forming metacercarial cysts in the flesh
Cats and dogs are infected by eating raw trout or salmon
Prepatent period is 6 days |
|
|
Term
| Clinical signs of "salmon poisoning" Nanophyetus salmincola? |
|
Definition
Clinical signs
The flukes are fairly benign, causing only a catarrhal enteritis
The flukes carry a rickettsia, Neorickettsia helminthoica, which causes “Salmon Poisoning” in dogs
Severe disease affecting only dogs
raccoons may show a transient fever
Characterized by vomiting, fever, diarrhea, lymphadonopathy, leucopoenia, thrombocytopoenia and anorexia
90% mortality in untreated dogs |
|
|
Term
| How to diagnose Nanophyetus salmincola? |
|
Definition
Diagnosis is by sedimentation of feces
Egg has operculum and measures 50 - 80 microns long
Clinical signs of salmon poisoning in endemic area |
|
|
Term
| Heterobilharzia Americana (blood fluke)!!! |
|
Definition
A blood fluke (liver & intestinal veins) of the raccoon reservoir
Dogs acquire it while swimming
Cercariae penetrate the dog’s skin
This fluke is unusual in that it has separate sexes |
|
|
Term
|
Definition
| An intestinal trematode dogs acquire by eating frogs or tadpoles |
|
|
Term
| !!! Tapeworms of dogs and cats!!! |
|
Definition
Platyhelminthes; Cestoda
Scolex holdfast
Ribbon-like, segmented body |
|
|
Term
| Tapeworms and their lifecycle: |
|
Definition
Hermaphroditic
One or two complete sets of male and female reproductive organs per segment
Single ovary with numerous testes;ooooo Adults live in small intestines of vertebrates
Indirect, simple life cycles
Variable number and kinds of intermediate hosts |
|
|
Term
| What are two major taxonomic groups of tapeworms? |
|
Definition
Cyclophylidea and Pseudophyllidea ooooo Two major taxonomic groups
Pseudophyllidea
Paired, slit-like bothria for holdfast
Median genital pore
Aquatic life cycle in which egg hatches in water and infects a copepod first intermediate host OOOOOOOOOOO Cyclophyllidea
Four round suckers for holdfast
Lateral genital pore
Unhatched egg ingested by intermediate host
Vertebrate or invertebrate |
|
|
Term
| Major species of tapeworms affecting cats and dogs? |
|
Definition
Major Tapeworms of Pets
Pseudophyllidea
Spirometra mansonoides (dogs and cats)
Cyclophyllidea
Dipylidium caninum (dogs and cats)
Taenia spp. (dogs and cats)
Echinococcus spp. (dogs and cats)
Usually diagnosed by routine fecal flotation with some exceptions
As a general rule, adult tapeworms are not particularly harmful to the final host
Can be deadly to an intermediate host |
|
|
Term
| Spirometra mensenoides characteristics? |
|
Definition
Order Pseudophyllidea
Adults live in the small intestine of felids & canids
Well established in the southeastern U.S.
Second most common tapeworm of cats in Florida
Seen less commonly in dogs
Cats and dogs are infected by hunting and eating intermediate hosts
Reptiles, small mammals and amphibians
Prepatent period is 18 - 30 days |
|
|
Term
| Pathology of Spirometra mansenoides |
|
Definition
Pathology
Enteritis and low grade fever caused by adults
Tissue destruction by sparganosis in improper second IH |
|
|
Term
| Spirometra namsenoides diagnosis? |
|
Definition
Diagnosis
Fecal flotation
Abundant eggs are shed in the intestine thus are mixed in the feces.
Golden brown operculated eggs (55 –65 microns)
Typically do not see proglottids in/on feces
Sometimes the entire worm is vomited |
|
|
Term
| Treatment and prevention of Spirometra Mansonoides? |
|
Definition
Treatment and Prevention:
A single dose of praziquantel at 20 mg/kg usually is effective
Note this is a higher dose than labelled for cyclophyllidean cestodes
Keep cats and dogs from hunting and eating their prey |
|
|
Term
| What are publick health concenrs with spirometra mansonoides? |
|
Definition
Public health considerations
Humans can become infected with a sparganum, i.e. is a 2nd intermediate host
Most commonly manifests as a painful subcutaneous nodule
Rarely a more serious cerebral or ocular sparganosis may occur |
|
|
Term
|
Definition
Order Cyclophyllidea
Adults in felids and canids
Same species in felids and canids
Inhabit small intestine
Two complete sets of reproductive systems per mature proglottid
World wide in distribution
Prepatent period = 18 days |
|
|
Term
| How do dogs and cats become infected with dIPILIDIUM CANINUM? |
|
Definition
By swallowing fleas that contain cysticercoids
NOT from the flea biting the dog or cat!
Fleas become infected as larvae by eating D. caninum eggs |
|
|
Term
| Pathology of Dipilidium caninum? |
|
Definition
Causes itch on perineum.
Competes slightley for nutrition, but not particularly damaging |
|
|
Term
| How can we diagnose Dipilidium Caninum? |
|
Definition
Diagnosis:
Observe proglottids crawling on perineum or on surface of feces.
Confirm by breaking egg packets out of proglottids and floating them or just teasing apart a proglottid in saline
These contain up to about 30 eggs/packet |
|
|
Term
| What is treatment and control protocol for Dipilidium caninum? |
|
Definition
Use either praziquantel or epsiprantel at FDA-approved single dose
Epsiprantel: cats 1.25 mg/kg; dogs 2.5 mg/kg
Praziquantel: 5 mg/kg for both
Flea control is a must |
|
|
Term
| What are public health concerns with Dipilidium Caninum? |
|
Definition
Humans may become infected by swallowing an infected flea
Mainly seen in children
Usually asymptomatic
Few reports of abdominal pain, diarrhea, and anal pruritus |
|
|
Term
| What are Taenic Cestodes? |
|
Definition
Several closely-related genera of Cyclophyllidean cestodes with a vertebrate intermediate host
Usually have a herbivore intermediate host and an carnivore final host
Omnivores may fall either way |
|
|
Term
| What are two most important genera of Taenid Cestodes? |
|
Definition
Taenia
The various species of this genus are more host specific in both DHs and IHs than Dipylidium and Spirometra
Echinococcus
The species of this genus have a broader range of herbivore/omnivore intermediate hosts than Taenia and use canids as final hosts |
|
|
Term
|
Definition
Order Cyclophyllidea
Species of this genus are more host specific in both DHs and IHs than Dipylidium and Spirometra. |
|
|
Term
|
Definition
Cycles between canids and rabbits.
Cysticerci are in the peritoneal cavity of IH
Cosmopolitan
Adults in small intestine |
|
|
Term
| How can dogs get Taenia pisiformis? |
|
Definition
Dog hunts and catches rabbit and eats it.
Cysticerci digested free, attach to mucosa of small intestine after scolex everts. |
|
|
Term
| Pathology of Taenis pisiformis |
|
Definition
Most species of Taenia do not cause disease, but all steal nutrients.
May have damage to IH due to cysticerci |
|
|
Term
| How to diagnose Taenia pisiformis? |
|
Definition
See proglottids in the feces or on perineum.
Tease proglottids apart in saline and examine eggs.
Eggs of all taeniids look identical and appear to have a radiating outer wall, hexacanth about 25-40 microns.
Eggs will float. |
|
|
Term
| What is treatment of Taenia pisiformis infestation? |
|
Definition
Use the same protocol as for Dipylidium for all of the taeniid tapeworms (Droncit or Cestex)
OOOO > Use either praziquantel or epsiprantel at FDA-approved single dose
Epsiprantel: cats 1.25 mg/kg; dogs 2.5 mg/kg
Praziquantel: 5 mg/kg for both
Flea control is a must |
|
|
Term
|
Definition
Echinococcus granulosus.
Canid to sheep usually (zoonotic).
Echinococcus multilocularis.
Dog or cat to rodents usually.
Cyst is the most damaging and complex – hydatid cysts.
Life cycle same for Taenia except for hyadatid cyst. |
|
|
Term
| Pathology of Echinococcus spp? |
|
Definition
Pathology:
Adults are not pathogenic.
Hydatid cysts are very damaging to the intermediate hosts as they can destroy normal organs as liver, lung and brain through pressure necrosis. |
|
|
Term
| Diagnosis of Echinococcus? |
|
Definition
See proglottids in feces: if in sheep country, then purge the gut, look for the tiny adults.
This is a zoonotic threat hydatids develop in people.
Remember the eggs look like Taenia. |
|
|
Term
| Treatment of Echinococcus infections? |
|
Definition
Same drugs used for other tapeworms work on adults, namely Droncit and Cestex.
Albendazole has some effect on the hydatids. |
|
|
Term
| !!!Acanths of dogs and cats? |
|
Definition
Few species in dogs and cats anywhere in world
Retractable spiny proboscis.
Adults live in small intestine
Indirect life cycle
Intermediate hosts – arthropods
Separate sexes |
|
|
Term
| What is the one specie of Acanths that is important for veterinarians in North America? |
|
Definition
Only one species normally lives in dogs in North America.
Macracanthorhynchus ingens
This uses millipedes as IH
Dogs are poor hosts and the acanths pass spontaneously
No species reported from cats in North America |
|
|
Term
| Can any drugs treat Acanths in dogs? |
|
Definition
No proven drugs for acanths.
Diagnosis by fecal flotation. |
|
|
Term
| Superfamily Filaroidea? (heartworm) |
|
Definition
These are usually long and slender worms
Lack prominent identifying characteristics
Vector transmitted
Male identified by a corkscrew-shaped tail |
|
|
Term
|
Definition
Dirofilaria immitis is the dog heartworm
Infects the pulmonary arterial system and right heart |
|
|
Term
| What are the primary hosts for Dirofilaria Immitis? |
|
Definition
Primarily a parasite of wild and domestic canids belonging to the genus Canis.
Dog
Wolf
Coyote |
|
|
Term
| Other species regularly infected by Dirofilaria? |
|
Definition
Cat
Is the prevalence of feline infection truly on the increase?
Has increased surveillance identified pre-existing foci of infection?
Ferret
California Sea Lion |
|
|
Term
| Other animals rarely infected with Dirofilaria immitis? |
|
Definition
Variety of other wild carnivores:
Canidae other than Canis spp., especially foxes
Felidae - tiger, jaguar, and other small cats
Ursidae - various species of bear
Procyonidae - raccoon, coatimundi, crabdog
Mustelidae - otter
Humans |
|
|
Term
| Main points about Dirofilaria life cycle? |
|
Definition
In mosquito
microfilaria è L3
2-3 weeks
In dog
L3 è adult worm è microfilaria
6 months |
|
|
Term
| Key events of Dirofilaria life cycle in a dog? |
|
Definition
L3 è L4 @ 3-12 days post-infection
Subcutaneous near site of mosquito bite
L4 è L5 @ 45-70 days post-infection
Muscle fascia of abdomen and thorax
ooo>Immature worms reach the heart & pulmonary arteries by 75-120 days post-infection.
Adults sexually mature by 6-7 months post-infection.
Microfilaremia appears
Antigenemia appears |
|
|
Term
| Key clinical signs od Dirofilaria? |
|
Definition
Nothing
Exercise intolerance
Weight loss
Chronic cough
Ascites
Hemoptysis |
|
|
Term
| Primary screening tests for Dirofilaria? |
|
Definition
Primary screening tests
Tests for microfilariae (mf)
Tests for antigens
Other diagnostic aids
Radiology
Echocardiography |
|
|
Term
| What is a key objective of diagnostic testing for Dirofilaria? |
|
Definition
| The objective of diagnostic testing is to identify dogs infected with cardiac stages of Dirofilaria immitis, i.e., those stages susceptible to treatment with melarsomine dihydrochloride. |
|
|
Term
| What are some tests for microfilaria of Dirofilaria? |
|
Definition
Non-concentration
Direct smear
Microhematocrit
Concentration
Modified Knotts
Membrane filtration
OOOO> The American Heartworm Society recommends that a concentration test be used when screening for microfilariae
The sensitivity of heartworm testing is reduced by about 20% if a direct smear is substituted for a concentration test as the only screening test for heartworm in dogs. |
|
|
Term
| What are some other microfilaria that may interfere with testing for Dirofilaria? |
|
Definition
Dirofilaria immitis
Dipetalonema reconditum
Less common than reported earlier
Decrease prevalence due to heartworm prevention with macrolides?
Adults are harmless subcutaneous parasites
Flea transmitted
Several other filarids of wildlife rarely infect dogs and are harmless |
|
|
Term
| What are some of the problems with test for microfilariae? |
|
Definition
~40% of heartworm infections are occult (no microfilariae in blood)
Macrolide-sterilized worms
Immune mediated occult
Only one sex present
Only immature worms present
Antigen tests detect many occults |
|
|
Term
| Antigen tests vs. tests for microfilariae? |
|
Definition
Antigen tests are significantly more sensitive than concentration tests for microfilariae at all worm burdens.
10% more sensitive with large numbers of heartworms
50% more sensitive with low numbers of heartworms
OOO> Not all microfilaremic dogs are antigen positive.
Antigens may be “sequestered” in about 1% of microfilaremic infections. |
|
|
Term
| What are properties of a modern antigen test? |
|
Definition
Very specific
Virtually 100%
Most false positives are due to technical error, especially poor washing technique with microwell tests.
Moderately sensitive
Sensitivities usually 75-90% (in Florida)
Sensitivity reduced with:
Low worm burdens (<5 female worms)
Absence of gravid female worms
Male worms only
Immature worms
Cold reagents – allow refrigerated test kits to warm up before use! |
|
|
Term
| How does antigen sensitivity vary with worm burden? |
|
Definition
1-2 worms 45%
3-5 worms 84%
6-10 worms 89%
11-20 worms 99%
>20 worms 100% |
|
|
Term
| When to test a dog for heartworm initially? |
|
Definition
Initial testing not necessary for puppies < 6 months old
Start on macrolide prophylaxis
Retest in 6-12 months for antigens only |
|
|
Term
| What is the protocol for HW testing of older dogs? |
|
Definition
Older dogs
Test when first seen and start heartworm prophylaxis if negative.
Test for both antigen & mff
Retest in 6-12 months for antigen only
Advise owner that their dog is not considered successfully started on prophylaxis until the second test is negative. |
|
|
Term
| How to test a symptomatic dog? |
|
Definition
First test for microfilariae
If amicrofilaremic, test for antigens
If also negative for antigens and clinical signs/history warrant, use radiology or echocardiography. |
|
|
Term
| What are radiographic signs of a HW positive animal? |
|
Definition
Lobar pulmonary arteries
Enlarged & tortuous
Pruned & taper lost
Emboli
Main pulmonary artery segment enlarged
Hazy lung parenchyma |
|
|
Term
| What are 4 steps in HW treatment? |
|
Definition
Evaluate and classify the patient
Kill adult worms
Eliminate microfilariae
Administer prophylaxis |
|
|
Term
| Preadulticide evaluation- 4 steps? |
|
Definition
Physical examination
Clinical laboratory data
Thoracic radiographs
Antigen test |
|
|
Term
|
Definition
Organic arsenicals
Melarsomine (Immiticide)
Long term (2.5-3 years) administration of ivermectin/pyrantel pamoate will clear most heartworms from most dogs
Worms start to die after 18 months or so
Not a replacement for Immiticide – use when immiticide not feasible
Sick dogs
Owner unwilling to bear the cost |
|
|
Term
| What are the signs that thromboembolic disease is going to happen upon treatment of HWs? |
|
Definition
| "A strongly positive antigen test accompanied by radiographic signs of extensive pulmonary vascular disease are indicative of an increased risk of adulticide-induced thromboembolic complications." |
|
|
Term
|
Definition
Organic arsenicals
Melarsomine (Immiticide)
Long term (2.5-3 years) administration of ivermectin/pyrantel pamoate will clear most heartworms from most dogs
Worms start to die after 18 months or so
Not a replacement for Immiticide – use when immiticide not feasible
Sick dogs
Owner unwilling to bear the cost |
|
|
Term
| What is long time Ivermectin tx for HW? |
|
Definition
Long term ivermectin
In general this approach should not be used in dogs with clinical signs of heartworm disease or in very active dogs
May be of some benefit for
Dogs too sick to tolerate melarsomine
Owner unwilling to bear the cost of melarsomine therapy
Best if used in combination with doxycycline therapy for removal of Wolbachia endosymbionts
Ivermectin and doxycycline administered periodically over 36 weeks resulted in a 78% reduction in adult worm numbers
Administer ivermectin monthly year round and repeat a one month course of doxycycline every 3-4 months |
|
|
Term
|
Definition
An extremely acute form of heartworm disease
Caused by a mass of worms obstructing blood flow through the tricuspid valve
Large number reached the heart over a short period of time
Heart cannot expand to accommodate the worm load as when worms arrive in a “trickle” |
|
|
Term
| What clinical signs of Caval Syndrome? |
|
Definition
Signs include
Acute, sudden collapse
Tricuspid murmur
Jugular pulse
Hemoglobinuria due to intravascular hemolysis
May or may not be microfilaremic or antigenemic |
|
|
Term
| How is medical emergency caval syndrome treated? |
|
Definition
treated by immediate surgical removal of adult worms via the jugular vein using rigid or flexible alligator forceps
Follow up with melarsomine once dog has recovered to remove unreachable worms |
|
|
Term
| When is surgical removal of HW performed? |
|
Definition
-non-caval syndrome dogs only, Fluoroscope-guided flexible alligator forceps may be used to remove some of the adult worm burden from the pulmonary artery
Reduces the risk of thromboembolic complications following subsequent melarsomine treatment |
|
|
Term
| How to properly administer Melarsomin (Immiticide)? |
|
Definition
Therapeutic index about 3
Nearly 100% efficacious
Administered as two IM injections 24 hours apart
Injected deep into lumbar muscles
Pay close attention to manufacturer’s recommendations as to maximum injection volume & needle size |
|
|
Term
| What are the alternatives to treatment with Melarsomine of severely HW infected dogs? |
|
Definition
Alternative for severely diseased dogs
One IM injection for partial worm kill
Give the full 2 dose treatment a month or two later
Many veterinarians routinely use this method for its greater efficacy & safety |
|
|
Term
| What are complications of Melarsomine treatment? |
|
Definition
Injection site reactions
Soreness
Swelling, heat and pain at the injection site
Reluctance to move
Sterile abscessation
Neurologic complications from injection are rare
May manifest as hindlimb ataxia, paraparesis, urine retention, fecal incontinence, flaccid tail
Presumably swelling presses on nerve roots or the drug directly irritates nerve roots
Recovery may not be complete
Prevent reactions by paying close attention to injection technique
Occurrence
Begins 1 week after melarsomine treatment
At risk for 4 weeks or more |
|
|
Term
| What are the signs of pulmonary thromboembolism? |
|
Definition
Signs
Depression
Fever
Cough
Hemoptysis |
|
|
Term
| How to tx and prevent pulmonary thromboembolism? |
|
Definition
Treatment
Corticosteroids
Strict rest
Prevention
Restricted exercise for 1-2 months after treatment
Prophylactic use of corticosteroids or aspirin is discouraged |
|
|
Term
| How to use Ivermectin pretreatment prior to giving Melarsomine? |
|
Definition
Monthly doses of ivermectin administered for 2-3 months prior to adulticidal treatment with melarsomine will eliminate young worms not susceptible to melarsomine
Melarsomine is not very effective against worms less than 4 months old |
|
|
Term
|
Definition
Endosymbiotic bacteria of the genus Wolbachia
Important in the survival of many filarial nematodes
May also play a role in the pathogenesis of heartworm disease |
|
|
Term
|
Definition
Prolonged doxycycline treatment (10mg/kg b.i.d. for four weeks)
Appears to hasten the spontaneous death of adult worms
Reduce the severity of clinical disease
Reduce complications following treatment with melarsomine.
Removes ~ 90% of Wolbachia organisms from the adult worms
Level of infection remains low for 3-4 months
Best if administered during the month preceding melarsomine treatment
Combining 2-3 months of pretreatment with ivermectin with 1 month of pretreatment with doxycycline markedly reduces complications of melarsomine treatment |
|
|
Term
| How can we confirm that adulticide treatment was successful? |
|
Definition
Successfully treated dogs seroconvert to negative by about 12 weeks after adulticidal treatment.
A positive test before this time is confounded by antigens released from dead worms. |
|
|
Term
| Elimination of Microfilariae? |
|
Definition
| Extra-label use of 50 mcg/kg ivermectin not less than 3 weeks after arsenical treatment is efficacious |
|
|
Term
| What are problems with giving a high dose Ivermectin? |
|
Definition
Marginally safe in collies & aussies
Shock-like reaction may occur in any dog having a high microfilaremia.
Caused by rapid death of large numbers of microfilariae
Treat with corticosteroids and parenteral fluids |
|
|
Term
| What can be an alternative to Ivermectin tx for Microfilariae? |
|
Definition
Administration of macrolides at their respective doses approved for heartworm prevention will render nearly all dogs amicrofilaremic in 6-9 months
Ivermectin
Milbemycin
Moxidectin
Selamectin
OooooSimply start dogs on prophylaxis without any attempt at microfilaricidal therapy.
Dogs should be hospitalized for first dose as a precaution against the rare shock-like reaction.
Greatest risk is with milbemycin - the most potent microfilaricide at prophylactic doses
Signs include lethargy, inappetence, salivation, retching, defecation, pale mucous membranes and tachycardia
Treat with parenteral fluids and one or two shock therapy doses of glucocorticosteroids
Some veterinarians use prophylactic steroids at this time. |
|
|
Term
| Chemoprophilaxis against HW infections? |
|
Definition
Semi-annual macrolides
Moxidectin (ProHeart 6)
Monthly macrolides
Ivermectin (Heartgard, Iverheart)
Milbemycin (Intecepter, Sentinel)
Moxidectin (Advantage Multi, ProHeart)
Selamectin (Revolution) |
|
|
Term
| What is "window of vulnerability" in HW disease? |
|
Definition
Macrolides reliably kill all larvae that are 2 months or less post-infection as well as many at 2-3 months
Microfilaremia and/or antigenemia do not appear until about 6 months post-infection.
Larvae more than 2 months, but less than 6 months, post-infection can neither be diagnosed nor entirely prevented.
The owner should be advised that a dog more than 8 weeks of age is not successfully started on prophylaxis until it tests antigen-negative 6 to 12 months later. |
|
|
Term
| Timing of prophylaxis against HW? |
|
Definition
Heartworm is seasonal except in the tropics and subtropics.
Year round transmission in the continental U.S. in parts of southern California, extreme southern Texas, and Florida south of Interstate Highway 4.
Pharmaceutical companies and their minions strongly promote unnecessary year round prophylaxis, even in cold climates
Claims it improves client compliance
As a general guideline, prophylaxis must be administered
Within as month of the beginning of the local mosquito season in the spring
Continued for at least 1 month following the first hard freeze of the winter |
|
|
Term
| Feline Dirofiliraisis, is it common? |
|
Definition
Prevalence is about 1/10th that of dogs within a given locality
Only a small number of worms are usually present, but even small numbers are life-threatening
Microfilaremia is not common and persists for less than 1 year |
|
|
Term
|
Definition
Infection is self-limiting, with adult worms dying after two or three years
Disease is more severe if present
Diagnosis is difficult
Treatment is difficult |
|
|
Term
| Signs of HW disease in cats? |
|
Definition
Most infected cats are asymptomatic
Coughing, gagging, dyspnea, and/or vomiting unrelated to eating
Asthma-like syndrome (Heartworm Associated Respiratory Disease)
Caused by the inflammatory response to
Newly arrived (4 month old) worms
Death of newly arrived worms
Acute thromboembolism and sudden death
Caused by the death of older, larger fully mature worms |
|
|
Term
| Are there any tests to check for HW in cats? |
|
Definition
Difficult because
Microfilaria & antigen tests lack sensitivity
Antibody tests lack specificity |
|
|
Term
| Is microfilaremia common in cats and how can we diagnose it? |
|
Definition
Microfilaremia
Appears in only about 50% of cats
Transient (1-2 months)
Positive test for microfilariae usually means heartworms are present
Negative test microfilariae does not rule out the presence of heartworm |
|
|
Term
| Is antigenemia common in cats with HW and how can we diagnose it? |
|
Definition
Antigenemia
Detectable in <30% of naturally infected cats
Positive antigen test usually confirms the presence of heartworm
Negative tests for antigen does not rule out presence of heartworm |
|
|
Term
| Do antibody tests to check for HW in cats exist? |
|
Definition
Antibody test is sensitive but lacks specificity
Remains positive for an extended time following the death of all worms
Positive antibody test does not confirm the presence of adult heartworm
Positive antibody test confirms only prior exposure to heartworm
Negative antibody test usually means heartworms are absent |
|
|
Term
| Is HW dz treatable in cats? |
|
Definition
Heartworm is essentially an untreatable disease in cats
Treatment with arsenicals is fraught with risk
Fatalities from embolism are common
Better not to treat cats since infection is self-limiting |
|
|
Term
| Can we prevent HW dz in cats? |
|
Definition
Macrolides are highly effective in preventing feline heartworm
Milbemycin 500 mcg/kg
Ivermectin 24 mcg/kg
Selamectin 6 mg/kg (topical)
Which cats need prophylaxis
Outdoor cats in endemic areas
Selected indoor cats? |
|
|
Term
| Do any other species get HW prevention? |
|
Definition
| Ferrets, California sea lions and a number of captive wild mustelid, canid, and felid species should be on macrolide prophylaxis |
|
|
Term
| Are human HW infections common? |
|
Definition
Human infection
Rare and self-limiting
May result in a transient pulmonary granuloma
Radiographic “coin lesion” resembles a pulmonary carcinoma
Triggers an unnecessary lung biopsy, especially for older, heavy smokers |
|
|
Term
| Other Dirofilaria parasites that affect humans? |
|
Definition
Human infection
Several human infections once attributed to D. immitis are now known to be the result of infection with other species of Dirofilaria
Larvae of Dirofilaria tenuis (raccoons) may be found in the anterior chamber of the human eye
Most prevalent in southeastern Florida
Dirofilaria repens (a subcutaneous parasite of dogs in eurasia) may cause skin nodules in humans in that region |
|
|
Term
| 1. What are major nematodes of cats and dogs? |
|
Definition
Phylum Nematoda; various superfamilies
Characteristics
Commonly called roundworms
Some are animal parasites
many more are not
plant parasitic
free-living bacterial feeders in the soil |
|
|
Term
| 2. Who has a "tube within a tube" body plan? |
|
Definition
Nematodes: Tube Within a Tube” body plan
Tubular body with tapered ends
Tubular reproductive and digestive systems
Tubular shape maintained by hydrostatic pressure like a water balloon |
|
|
Term
| 3. What are three major characteristics of nematodes? sexes___, ___ cuticle, __ digestive system? |
|
Definition
Digestive system complete
Sexes separate
External cuticle |
|
|
Term
| 4. Life cycle of Nematodes? |
|
Definition
Simple terminology, but life cycles may be complex
Egg--> L1-->L2-->L3-->L4-->L5 (adult)
4 molts occur
May or may not use intermediate hosts or transport hosts
1) Patterns of development
in soil after L1 hatches (L3 infective)
in soil within egg (L1 or L2 infective)
within IH (L3 or L4 infective) |
|
|
Term
| 5. What are infective stages of Nematodes? |
|
Definition
All superfamilies except the following use the L3 (= the L3 Rule)
Trichuroidea use L1
Ascaroidea use L2
Dioctophymoidea use L4 |
|
|
Term
| 6. Does 1 egg mean 1 adult worm in Nematodes? |
|
Definition
yes: No asexual multiplication
1 egg can become only 1 adult worm |
|
|
Term
| 7. Important genera of Nematoda? |
|
Definition
Strongyloides Dog & Cat
Ollullanus Cat
Filaroides Dog
Aelurostrongylus Cat
Ancylostoma Dog & Cat
Uncinaria Dog & Cat
Physaloptera Dog & Cat
Spirocerca Dog
Toxocara Dog & Cat
Toxascaris Dog & Cat
Dirofilaria Dog & Cat
Dipetalonema Dog |
|
|
Term
| 8.The BIG THREE of Nematodes in vet med? |
|
Definition
Ascarids
Hookworms
Whipworms |
|
|
Term
| 9. Which nematodes are inportant in Pet Health and which in human health? |
|
Definition
Ascarids
Hookworms
Whipworms |
|
|
Term
| 10. Describe superfamily of Nematodes-Ascaroidea? |
|
Definition
Superfamily Ascaroidea:
Large robust roundworms
Three big lips
No bursa on males
Thick shelled egg that does not hatch in the environment
Egg containing the L2 is infective
Larvae migrate extensively in host
Typically through the liver and lungs |
|
|
Term
| 11. Main Ascarids of cats and dogs? |
|
Definition
Toxocara canis (dogs)
Toxocara cati (cats)
Toxascaris leonina (dogs & cats)
Baylisascaris procyonis (dogs)
OOOOOO>Adults live in small intestine
All but B. procyonis are cosmopolitan
All have very resistant eggs = remain infective for years |
|
|
Term
| 12. Toxocara canis (nematode of pets)? |
|
Definition
Cosmopolitan distribution
Clinically the most important
Most puppies born infected
Heavy infections common
Major routes of infection are transplacental (neonates) and ingestion of infective eggs (older pups and adults) |
|
|
Term
| 13. What are most important routes of infection by Toxocara canis? |
|
Definition
Hepatic-tracheal migration follows ingestion of eggs or placental infections (pups born with larvae in liver)
Less important routes include ingestion of colostrum and paratenic hosts
Larvae remain in the gut when acquired from colostrum or paratenic hosts
Prepatent period is 28 – 35 days for ingestion of infective eggs or larvae in colostrum
Transplacental route is 21 days
Ingestion of larvae via a paratenic host is 2 weeks
Strong age-related immunity
Due to pronounced liver-lung migration
Most patent infections are seen in puppies |
|
|
Term
| 14. Toxocara cati? (Nematode of cats) |
|
Definition
Toxocara cati (cats)
Cosmopolitan distribution
Clinically less important than T. canis, however
Lacks highly efficient placental transmission
Cats are more fastidious than dogs
Infections occur later in life & are less severe |
|
|
Term
| 15. What are routes of infection by Toxocara cati? |
|
Definition
Routes of infection include ingestion of infective eggs, paratenic hosts and colostrum (major route for young)
Hepatic-tracheal migration only occurs following ingestion of eggs
Larvae remain in the gut when acquired from colostrum or paratenic hosts
Prepatent period about 55 days |
|
|
Term
| 16. Can animals develop immunity to Toxocara cati? |
|
Definition
Weak age related immunity
Less liver-lung migration
Cats of any age may pass eggs |
|
|
Term
|
Definition
Toxascaris leonina (dogs & cats
Cosmopolitan, but limited to cold climates
Less important
Not as prevalent as T. canis or T. cati
More common in zoological collections in big felids |
|
|
Term
| 18. What are routes of infection by Toxoscara leonina? |
|
Definition
Infection occurs by
ingestion of infective eggs
ingestion of larvae in paratenic hosts
Lacks placental or colostral transmission
Infections occur later in life & are less severe |
|
|
Term
| 19. Is their prepatent period and is there age-related immunity to Toxoscaris leonina? |
|
Definition
Prepatent period
10 weeks from ingestion of eggs
8 weeks from ingestion of a paratenic host such as a mouse
Weak age-related immunity
No liver-lung migration
Life cycle is all enteric, whether infection is via eggs or larvae in paratenic hosts
Persistent reinfection can be problematic in adult animals |
|
|
Term
| 20. Baylisascaris procyonis? |
|
Definition
Baylisascaris procyonis (raccoons, unusual in dogs)
Rare accidental parasite of dogs, especially in Florida
Much more prevalent in the northeast, midwest, great lakes states, and the west coast
Prevalence in adult raccoons may reach 90% in the above regions but are uncommon in the southeast
A few reports of CNS disease in dogs due to larval migrations, otherwise canine infections are asymptomatic
Significant primarily as a public health hazard
Can cause ocular and CNS disease, especially in children |
|
|
Term
| 21. What are clinical signs of ascarid infection? |
|
Definition
Clinical signs of ascarid infections
Unthrifty, pot-bellied puppies or kittens
Vomiting and/or diarrhea
Pneumonia or seizures
Intestinal obstruction, intussusception or rupture
Obstructive jaundice |
|
|
Term
| 22. What is the best way to diagnose Ascarids in pets? |
|
Definition
Eggs recovered from fecal flotation
Toxocara spp. & B. procyonis eggs are virtually identical
Round, to oval, rough-walled, dark brown, approximately 75-90 microns in diameter
T. leonina eggs are oval, smooth walled, some 80-90 microns and have a clear shell lined with a wrinkled membrane |
|
|
Term
| 23. How to diagnose Ascarids based on appearance of actual worms in feces? |
|
Definition
Diagnosis
10-18 cm pinkish-white adult worms having 3 lips passed in feces or vomitus |
|
|
Term
| 24. What is the best tx for Ascarids? |
|
Definition
Any nematocide approved for ascarids
Persistent reinfection can be a problem with T. cati and T. leonina as there is little acquired immunity
T. leonina can be a problem in big cats in zoos
Arrested larvae accumulate in gut wall
FBZ kills ~95% of larvae |
|
|
Term
| 25. What is prevention of Ascarids? |
|
Definition
Immunologic maturity controls T. canis but not T. cati or T. leonina
Patent infections often occur in nursing bitches & queens
Good diet
Minimize stress & crowding
Good sanitation (pick up feces 2X weekly)
Anthelmintic treatment |
|
|
Term
| 26. What is CDC standard for treatment of puppies and adult dogs for Ascarids? |
|
Definition
Suppress fecal egg output by treating bitch & litter at 2, 4, 6, & 8 weeks post partum
Significant fecal egg output normally begins at 3 weeks post whelping
Begin at 3 weeks if hookworm is rare
Some recommend continuation to 12 weeks, then monthly until 1 year
Pyrantel pamoate is a good choice
Safe for puppies 2 weeks of age |
|
|
Term
| 27. What is CDC treatment scheme for cats for Ascarids? |
|
Definition
Suppress fecal egg output by treating queen & litter at 3, 5, 7 & 9 weeks post partum
No prenatal infections, so egg excretion begins later
Pyrantel pamoate is a good choice
Only feline-label product also contains praziquantel
Not for kittens <4 weeks or 1.5 lbs |
|
|
Term
| 28. Does HW preventative also preven ascarids? |
|
Definition
Regular heartworm prophylaxis for puppies in first year of life with a product solidly effective against ascarids as well
In most areas of U.S. dogs will be on a heartworm preventive that also prevents intestinal nematodes
Adult dogs & cats should be treated on the basis of a positive fecal exam
Not usually needed if on a heartworm prevention that also controls ascarids |
|
|
Term
| 29. What is the best way to treat a pregnant bitch who has Ascarids? |
|
Definition
50 mg/kg/day FBZ day from 40 of gestation until day 14 post partum
90% ascarid control, 99% hookworm control
Expensive - lab animal use only
300 mcg/kg ivermectin on day 0, 30, 60 of gestation and 10 days post whelping
Reduced adult T. canis worm burden in greyhound pups by 100%
Prevented shedding of eggs
Not for use in collies!
Selamectin at 10 and 40 days both before and after parturition
Reduces T. canis fecal egg counts in both pups and their dams, and adult worms in the pups |
|
|
Term
| 30. What are public health considerations when it comes to treating for Ascarids? |
|
Definition
Heavy infections can cause visceral larva migrans characterized by fever, cough, abdominal, hepatomegaly and eosinophilia
Larvae are killed in the lungs and never mature in the gut
Lighter infections may lead to larval invasion of the retina
Results in granulomatous of the retina, uveitis, and/or chorioretinitis
May result in focal or complete blindness of the affected eye
Baylisascaris procyonis can cause visceral, ocular or CNS disease
The raccoon, rather than the dog, is the primary source of eggs infecting humans
Larvae of B. procyonis have a strong propensity to migrate within the CNS
May cause severe CNS disease in a variety of animals, including humans
Children at greatest risk |
|
|
Term
|
Definition
Superfamily Strongyloidea
Large mouth and often with teeth
Direct life cycle
Prepatent period 2-3 weeks
Males have copulatory bursas
Head bent dorsally making “hook”
Adults live in small intestine
Worldwide distribution |
|
|
Term
| 32. What hosts and climate do hookworms like? |
|
Definition
Host specialists
Ancylostoma caninum (dogs)
Ancylostoma tubaeforme (cats)
Climate specialists
Ancylostoma brasiliense (warm climates)
Uncinaria stenocephala (cold climates) |
|
|
Term
| 33. What do adult hookworms look like? |
|
Definition
| 1 cm long adult worms inhabiting the small intestine |
|
|
Term
| 34. How do hookworms feed? |
|
Definition
| Adults attach to the intestinal mucosa and either suck blood or “plug feed” on liquefied tissue. |
|
|
Term
| 35. Do hookworms have teeth? |
|
Definition
The buccal cavity of A. caninum and A. tubaeforme have 3 pairs of teeth on each side
A brasiliense has only 1 pair of teeth
U. stenocephala has cutting plates instead |
|
|
Term
| 36. Are hookworms deadly? |
|
Definition
Ancylostoma caninum is the most important species
Regularly kills puppies in the Southeast
Rapidly builds up in large nubmers
Greatest propensity for blood sucking
Other species less pathogenic
Greater propensity for plug feeding
Less abundant |
|
|
Term
| 37. What are some main sources of infections by hookworms? |
|
Definition
Ancylostoma caninum is the most important species
Regularly kills puppies in the Southeast
Rapidly builds up in large nubmers
Greatest propensity for blood sucking
Other species less pathogenic
Greater propensity for plug feeding
Less abundant |
|
|
Term
| 38. What are minor sources of infection by Hookworms? |
|
Definition
Placental (A. caninum)
Paratenic hosts (all species)
These routes not considered in preventive programs |
|
|
Term
| 39. What are forms of hookworm disease from least sever to most? |
|
Definition
Placental (A. caninum)
Paratenic hosts (all species)
These routes not considered in preventive programs |
|
|
Term
| 40. What are clinical signs of a nuisance infection with hookworms? |
|
Definition
Placental (A. caninum)
Paratenic hosts (all species)
These routes not considered in preventive programs |
|
|
Term
| 41. Pathogenesis of nuisance Hookworm infection? |
|
Definition
Host immunity keeps the number of adult hookworms below the level at which disease occurs (“premunition”)
Arrested larvae accumulate in muscles
Muscle leak occurs constantly
Dead adult worms quickly replaced |
|
|
Term
| 42. TX of Nuisance hookworm infection? |
|
Definition
Treatment
Need for treatment questioned
Prevention
Sanitation & good nutrition
No compelling need for chemoprophylaxis
Most heartworm prophylaxis will also control hookworms
May see some worm eggs just before next monthly treatment is due |
|
|
Term
| 43. Clinical presentation of a chronic hookworm infection? |
|
Definition
Clinical Presentation
Adult dog, usually larger breed
Lives outdoors, often rural, lower socioeconomic household
Low grade anemia
Slight loss of weight/condition
Mild vomiting or diarrhea
Variable fecal egg count |
|
|
Term
| 44. Pathogenesis of a chronic hookworm infection? |
|
Definition
| Host immunity cannot keep the number of adult hookworms below the level at which mild disease occurs |
|
|
Term
| 45. What are some causes of reduced immunity? |
|
Definition
Poor diet
Poor sanitation
Stress
Concurrent disease
Genetics (?) |
|
|
Term
| 46. How to treat a chronic hookworm infection? |
|
Definition
Any modern anthelmintic effective against hookworms
Clean up the environment
“Sanitation & sunlight”
Hookworm larvae are short-lived in the soil (1-3 months)
Apply borax or rock salt to bare soil
Correct the cause of reduced immunity
Good diet & clean, stress-free environment
Treat any concurrent diseases |
|
|
Term
| 47. Prevention of hookworms is possible and easy. |
|
Definition
Good diet (“Purina Dog Chow®” or better)
Clean, dry, sunlit runs
Fecal pickup 2X weekly from yards
Eliminate stress and crowding |
|
|
Term
| 48. Chemoprophilaxis in tx of hookworms should be last resort? |
|
Definition
Chemoprophylaxis as a last resort and only if needed
Monthly INTERCEPTOR® or HEARTGARD PLUS® (or generic equivalents) for heartworm prevention is usually adequate |
|
|
Term
| 49. How does decompensated chronic hookworm infection look like? |
|
Definition
Like chronic hookworm disease but more severe
Like acute hookworm disease, but in adult animals instead of puppies
Treat & prevent like chronic hookworm disease
Pay special attention to stress, sanitation & diet |
|
|
Term
| 50. Clinical presentation of acute hookworm disease? |
|
Definition
Clinical presentation
Puppies near the age of weaning
Profound anemia (PCV < 20)
Black tarry to reddish brown feces
Pneumonia (?)
Many hookworm eggs on fecal flotation |
|
|
Term
| 51. What is pathogenesis of an acute hookworm disease? |
|
Definition
Pathogenesis
Massive infection by a second generation of worms
Offspring of colostrally-acquired worms plus pre-existing environmental contamination
Unrestrained blood sucking by adult worms due to lack of immunity |
|
|
Term
| 52. What is tx for acute hookworm infection? |
|
Definition
Treatment
Medical emergency
Fast acting, gentle anthelmintic such as pyrantel pamoate
Blood transfusion
Good nursing care
Most get well or die within 24 hours of treatment |
|
|
Term
| 53. Do you need to follow up on patients sent home after hookworm tx? |
|
Definition
Must follow up when sent home
Many infective larvae in environment
Many developing larvae in puppies
Clean up environment or move puppies to clean housing
Weekly pyrantel pamoate?
May switch to Interceptor or Heartgard Plus after 1st month |
|
|
Term
| 54. What to do to prevent Acute hookworm infections? |
|
Definition
Prevention
Good sanitation and parasite control so that large numbers of larvae do not accumulate
In the bitch
In the environment
CDC treatment scheme to prevent development of second generation worms |
|
|
Term
| 55. What are CDC regulations on how to treat bitch and litter for hookworms? |
|
Definition
Very high fecal egg output normally begins at 3 weeks post whelping
Treat at 2, 4, 6, & 8 weeks post whelping
Pyrantel pamoate is a good choice
Totally suppresses all fecal egg output |
|
|
Term
| 56. What is a clinical presentation of Peracute hookworm infection? |
|
Definition
Clinical Presentation
Very young puppies (~ 10 days old)
Profound anemia
Black tarry to reddish brown feces
No hookworm eggs on fecal flotation
Diagnosed on the basis of clinical signs |
|
|
Term
| 57. What is pathogenesis of Peracute Hookworm infection? |
|
Definition
Colostrally acquired infection is potentially lethal
Bloodsucking begins by 8 days of age
Blood supply depleted by 10 days of age
Prepatent period normally 14 days |
|
|
Term
| 58. How to tx peracute hookworm infestation? |
|
Definition
Treatment is like acute hookworm disease
Prevention is by treating “at risk” litters at 1 week of age with pyrantel pamoate or FBZ
May not be possible |
|
|
Term
| 59. How to get rid of larvae of hookworms int he environment? |
|
Definition
Spontaneously die in <2 months in warm weather
Larvae of Ancylostoma spp. (but not Uncinaria spp.) killed by hard freezes
Larvae killed by exposure to sunlight
Larvae osmotically dehydrated by borax or rock salt |
|
|
Term
| 60. What is cutaneous larva migrans and what causes it? |
|
Definition
Hookworm larvae travel: Superficial pruritic tracks on skin caused by larvae unable to penetrate the basement membrane
A. brasiliense is the most important cause
Normally self limiting or treated topically |
|
|
Term
| 61. What are trichuroids of dogs and cats? |
|
Definition
Superfamily Trichuroidea
Beaded esophagus
L1 is infective stage
Eggs when present have bipolar plugs
Species commonly seen in dogs and cats have a direct life cycle and no extra-enteric migration |
|
|
Term
| 62. Name two common Trichuroids? |
|
Definition
Trichuris vulpis
Caecum and colon of canids
Cosmopolitan & common
Trichuris campanula
Caecum and colon of cats
Neotropics and extreme southern Florida
Rare in U.S.
Capillaria plica
Urinary bladder of dogs
Uncommon
Capillaria feliscati
Urinary bladder of cats
Uncommon
Capillaria aerophila (fox lungworm)
Primarily a parasite of the frontal sinuses, trachea, and bronchi of foxes
Trichinella spiralis
intestinal tract (adults) and muscles (encysted L1s) of dogs
Rare |
|
|
Term
| 63. What is name for fox lungorm? |
|
Definition
Capillaria aerophila (fox lungworm)
Primarily a parasite of the frontal sinuses, trachea, and bronchi of foxes
Will infect the respiratory system of dogs, cats and a wide variety of other wild carnivorous mammals
Also called Eucoleus boehmi and Eucoleus aerophila
Worldwide distribution
Uncommon, but can be problematic on farms raising foxes for fur |
|
|
Term
| 64. Life cycle of Trichuroids? |
|
Definition
Eggs containing the L1 are ingested
Hatch & develop briefly in the mucosa of the small intestine
Eventually take up residence in the cecum
Complete development, mate and produce eggs that pass in the feces
Long prepatent period (74-90 days)
Eggs may survive many years in the environment |
|
|
Term
| 65. Trichuris sp? What are their ADULT WORM characteristics? |
|
Definition
Inhabit the caecum and spill over into the adjacent colon in heavy infections
Whip-like in appearance
long, thin anterior end
short, fat posterior end less than 1 cm long
Anterior end attached to cecal mucosa |
|
|
Term
| 66. What are clinical signs of Trichuroid (whipworm) infection? |
|
Definition
Bloodsucker
Long whiplike anterior end tunnels into cecal mucosa and lacerates a venule
Results in hemorrhagic typhlitis
Chronic mucoid to hemorrhagic large bowel type diarrhea
Weight loss
Moderate anemia
Vomiting |
|
|
Term
| 67. How can we diagnose a whipworm (Trichuroid) infection? |
|
Definition
Detection of trichuroid eggs by fecal flotation
Golden-brown, football-shaped eggs having a polar plug in either end |
|
|
Term
| 68. What other parasite's egg looks similar to Trichuroid (whipworm) egg? |
|
Definition
Rule out Capillaria spp. eggs
Smaller that whipworm (65 v.s. 75 microns)
Rough or netted rather than smooth egg shell
Clear rather than orange colored |
|
|
Term
| 69. Is centrifugation needed for fecal exam that detects Trichuroid eggs? |
|
Definition
Eggs can be hard to find
Do not float as easily as ascarid or hookworm eggs
Centrifugal sugar flotation may be more sensitive than passive NaNO3 flotation
Shed in small numbers at irregular intervals
Repeat fecal exams may be needed
90 day prepatent period in dogs
Disease may appear as early as 60 days
May have clinical signs appear before the long prepatent period has elapsed |
|
|
Term
| 70. How to tx Whipworm (Trichuroid) infection? |
|
Definition
Use any modern anthelmintic approved for control of whipworms
Note that pyrantel is not effective against whipworms |
|
|
Term
| 71. How to prevent Whipworms (Trichuroids)? |
|
Definition
Regular fecal examination and anthelmintic treatment, if indicated, to reduce egg shedding
Regular fecal pickup (2X weekly) to eliminate accumulation of eggs in the environment
Monthly milbemycin oxime (INTERCEPTOR) |
|
|
Term
| 72. Are there any human health issues with Trichuroids? |
|
Definition
No> The human whipworm, Trichuris trichura, does not infect dogs (or cats)
Dog (or cat) whipworms do not infect humans |
|
|
Term
| 73. How can environment be cleared of whipworm eggs? |
|
Definition
Cleanup of existing contamination with whipworm and ascarid eggs
Survive for years in environment if protected from direct sunlight
Contaminated soil:>
Till soil
Done once will bury about 90% of worm eggs
Done repeatedly will soon begin to uncover as many eggs as are buried
Remove topsoil
Cover contaminated soil with concrete or asphalt
These methods are obviously not compatible with lawns
Contaminated runs and cages
Bleach & soap wash of concrete runs & metal/fiberglass/plastic cages
Heat treatment (flame gun or steam cleaner)
Not for fiberglass/plastic cages
Bedding
Hot water wash and high temperature dry |
|
|
Term
|
Definition
|
|
Term
| 101. Protozoa: How many of them are known? |
|
Definition
Approx. 60,000 named species
50% extinct
approx. 21,000 free living protozoa
10,000 parasitic |
|
|
Term
| 102. Are protozoa Eukaryotes? |
|
Definition
Eukaryotic, single-celled (unicellular)
Nucleus
Mitochondria*
trichomonads: hydrogenosomes; Giarida: cryptons
Endoplasmic reticulum
Golgi apparatus |
|
|
Term
| 103. Are Protozoans able to move and what do they use for locomotion? |
|
Definition
Organelles of locomotion
Flagella
anterior, posterior, both
Giardia, trichomonads
Cilia
small flagella, can fuse to form membranes
Balantidium, rumen and cecal ciliates
Pseudopods
false feet, temporary extensions of cytoplasm
amoebae
Undulating ridges, subpellicular microtubules
movement by flexing and gliding
apicomplexans (Toxoplasma, Neospora, Babesia, etc) |
|
|
Term
| 104. How do protosoans reproduce? |
|
Definition
Protozoan reproduction
binary fission
asexual; longitudinal or transverse
multiple fission or schizogony
asexual; many new organisms formed
budding
asexual; bud from surface of parent
conjugation
not truly sexual; exchange of genetic information
followed by binary fission
syngamy or gametogony
sexual; union of similar (isogamy) or dissimilar (anisogamy) gametes |
|
|
Term
| 105. What is full classification of Protozoa? |
|
Definition
Kingdom: Protista
Phylum:
Sarcomastigophora
Apicomplexa
Ciliophora
Microspora |
|
|
Term
| 106. General characteristics of Phylum Sarcomastigophora? |
|
Definition
Distinct nucleus
Movement: most via flagella
Asexual reproduction – binary fission most common
sexual reproduction suggested – possibly form of conjugation
Direct & Indirect Life cycles
Direct: trichomonads, Giardia
Indirect: Leishmania, Trypanosoma |
|
|
Term
| 107. Describe the flagella of Sarcomastigophora? |
|
Definition
One or more flagella
Types
Phytoflagellates
free-living, plant-like
Zooflagellates
live in blood, lymph, digestive or reproductive tracts |
|
|
Term
| 108. Describe Trichomonads Giardia sp? |
|
Definition
Trichomonads, Giardia sp.
Movement: flagella and/or undulating membrane
Longitudinal binary fission
sexual reproduction unknown
Diagnosis
direct smear (trophozoites)
fecal flotation – Giardiacysts
PCR |
|
|
Term
| 109. What are Leishmania sp? |
|
Definition
Trypanosoma sp., Leishmania sp.
Movement: flagella, undulating membrane
Binary fission
sexual reproduction unknown
Diagnosis
Leishmania: serum testing, organ/skin biopsy
Trypanosoma: blood smear, serum testing |
|
|
Term
| 110. What is life cycle and hosts of Giardia? |
|
Definition
Direct Lifecycle
no intermediate host
World wide distribution
Hosts
mammals (man, dogs, cats, cows, goats, sheep, horses, rabbits, rodents) birds, amphibians
40 named species – 6 recognized; divided into complexes |
|
|
Term
| 111.Name some species of Giardia, which is most important? |
|
Definition
Giardia duodenalis is the most common)>
Recognized species
G. duodenalis
G. agilis
G. muris
G. ardeae
G. psittaci
G. microti |
|
|
Term
| 112. What are cysts and Trophozoites of Giardia? |
|
Definition
Cysts
environmentally resistant
infective stage, passed in feces
7-10 um, 4 nuclei
found in formed feces
Trophozoites
vegetative, reproducing stage
mucosal surface of small intestine
9-21um, 2 nuclei and sucking disc
4 pairs of flagella
found in diarrheic feces |
|
|
Term
| 113. What are clinical signs of Giardia? |
|
Definition
Clinical signs
majority asymptomatic
chronic infections
villus atrophy
intermittent diarrhea
loose, mucoid
not watery
can last weeks to months
Prevalence
more common in younger animals |
|
|
Term
| 114. How to diagnose Giardia? |
|
Definition
Diagnosis
zinc sulfate or sugar flotation (cysts)
direct smear (trophozoites)
ELISA |
|
|
Term
| 115. How to treat Giardia? |
|
Definition
Treatment
Dogs
metronidazole, albendazole, fenbendazole, quinacrine
Cats
metronidazole, quinacrine, furazolidone |
|
|
Term
| 116. What are major characteristics of Tritrichomonas foetus? |
|
Definition
Characteristics
3 anterior flagella
1 posterior, recurrent flagellum
avg. 15μm long x 9μm wide
UM ¾ length of cell
axostyle extends from posterior end
pseudocysts
longitudinal binary fission |
|
|
Term
| 117. What animals frequently get Tritrichomona foetus? |
|
Definition
CATS: > first reports of trichomonads in feline feces early 1900s
first implicated as causative agent of large bowel disease 1956
increasing reports since 1996
organisms recovered morphologically similar to Tritrichomonas foetus |
|
|
Term
| 118. What are clinical signs of feline Tritrichomona infection? |
|
Definition
Large-bowel disease
chronic diarrhea
blood and/or mucus
tenesmus
flatulence
irritated anus
fecal incontinence
soiling outside litter box
Transmission unknown
likely fecal-oral route
Chronic diarrhea
weeks, months, years
large bowel inflammation
Age of onset
avg. 9 mo. (range 0-24 mo.)
Diarrhea may relapse
Spontaneous resolution
after 2 years ?? |
|
|
Term
| 119. What part of GI tract do Trichomonasa like to go to? |
|
Definition
T. foetus lives in colon
adhere to epithelial cells
Feline Host(s)
male and female
domestic and purebred |
|
|
Term
| 120. How can we detect Trichomoniasis in cats? |
|
Definition
Direct fecal smear
Culture
Diamond’s media
InPouch TF® culture system
Polymerase chain reaction (PCR)
Colonic biopsy |
|
|
Term
| 121. Is there any treatment for Trichomoniasis? |
|
Definition
No approved treatment
Drugs that have demonstrated efficacy against T. foetus in cats:
enrofloxacin, metronidazole, fenbendazole
used in combination
ronidazole (not FDA approved)
Keep infected cats away from other cats
Do not allow litter box sharing |
|
|
Term
| 122. What are some non-pathogenic Trichomonas? |
|
Definition
Pentatrichomonas hominis
8 x 20um (avg)
3-5 anterior flagella
1 posterior flagellum
ooo>
Tetratrichomonas spp.
T. pavlovi (syn. bovis)
T. buttreyi
4 x 6um (avg)
4-5 anterior flagella
1 posterior flagellum |
|
|
Term
| 123. What are major characteristics of Tripanosoma cruzi? |
|
Definition
Parasites of all classes of vertebrates
blood and tissues
some intracellular
Majority transmitted by blood feeding invertebrates
Most do not cause disease
Kinetoplast
darkly staining
base of flagellum
Pleomorphic
Cytoskeleton
microtubules
Single nucleus |
|
|
Term
| 124. Who can serve as a host for Tripanosoma Cruzi and what is its vector? |
|
Definition
American Trypanosomiasis
dogs, cats, opossums, armadillos
reservoir hosts
Chagas Disease
humans
Vector : Reduviid bug
aka Triatomine, Kissing, Assassin Bug |
|
|
Term
| 125. What is epidemiology related to Tripanosoma Cruzi? |
|
Definition
Epidemiology
1910 Carlos Chagas
8-11 mil. human infections: Mexico, C. and S. America
Rare in US
Maryland, Georgia, Florida, Texas, New Mexico, California, Alabama, Virginia, Tennessee, Louisiana |
|
|
Term
| 126. Describe Tripanosomostigote? |
|
Definition
Trypomastigote
circulating blood
slender cell body, 16-20 um
pointed posterior
moderately long flagellum
subterminalkinetoplast
largest of all trypanosomes |
|
|
Term
| 127. Describe Amastigote of Tripanosoma? |
|
Definition
Amastigote
muscles, other tissues
spherical, 1.5-4 um
occurs in clusters |
|
|
Term
| 128. What does acute Chagas dz look like? |
|
Definition
weeks to months or asymptomatic
parasites in circulating blood
fever, swelling around site of parasite entry
Romaña’s sign
rarely severe inflammation of heart or brain |
|
|
Term
| 129. What does chronic Chagas dz look like? |
|
Definition
prolonged, asymptomatic
no parasites in circulating blood
20-30% develop severe disease
heart arrhythmia
dilated heart
immunosuppression can lead to ‘reactivation’ of disease
parasites again found in circulating blood |
|
|
Term
| 130. Does Tripanosoma infect dogs and what percentages of what kind? |
|
Definition
AKC Infection Surveys
sporting dogs – 51.6%
working dogs – 12.8%
lifestyle (outdoors, wildlife exposure, insectivorous)
breed popularity
50% acute deaths dogs <1 year old |
|
|
Term
| 131. What are clinical signs of dogs affected by Tripanosoma? |
|
Definition
most diagnosed during chronic stage
dilated, enlarged heart
arrhythmia
lethargy
respiratory difficulties
hepatomegaly
anemia |
|
|
Term
| 132.How can we diagnose Tripanosoma cruzi? |
|
Definition
Serological testing
TESA blot / Western blot
trypomastigote excreted – secreted antigen
ELISA
enzyme – linked immunosorbent assay
IFA
indirect immunofluorescence assay
IHA
indirect hemagglutination assay
Blood smear
only good for acute phase (trypomastigotes)
Xenodiagnosis
allow Reduviid bugs to feed on patient; look for trypanosomes 10-30 days later |
|
|
Term
| 133. Is there treatment for Tripanosoma cruzi? |
|
Definition
Most Experimental
low efficacy against chronic disease
harsh side effects
treatment over 2-3 months
benznidazole – acute disease
ravuconazole – parasitemia suppressed; no cure |
|
|
Term
| 134.Describe phylum Apicomplexa? |
|
Definition
Distinct nucleus
Movement: subpellicular tubules
microgametes (male) often flagellated
Apical complex
Orders:
Eucoccidiida
Piroplasmida |
|
|
Term
| 135. Name a list of Coccidia and which ones are considered classical coccidia? |
|
Definition
Eimeria and Isospora are the 2 classical;
Genera
Eimeria
Isospora
Cryptosporidium
Toxoplasma
Neospora
Hammondia
Sarcocystis |
|
|
Term
| 136. What reproducation is used by Eucoccidia? |
|
Definition
Asexual & sexual reproduction
sporogony
schizogony
gametogony
resistant oocysts released in feces of definitive host (DH |
|
|
Term
| 137. What are parasitic stages of Eucoccidia? |
|
Definition
Parasitic stages
DH: primarily in intestinal epithelial cells
Intermediate Host (IH): various locations |
|
|
Term
| 138. What is a life cycle of Eucoccidia? |
|
Definition
direct (no IH) and indirect (IH)
patent period
time oocysts shed in feces
prepatent period
time from ingestion of sporulatedoocyst until oocysts appear in feces |
|
|
Term
| 139. How can we diagnose Eucoccidia? |
|
Definition
fecal flotation (oocysts)
serology
immunochemistry |
|
|
Term
| 140. What is host range of Eimeria and Isospora? |
|
Definition
Stenoxenous
narrow host range
Worldwide distribution
Organ specificity
found in specific organ depending on species
Small or Large Intestine, Cecum, rarely liver, kidney
Monoxenous
parasitize one host (DH) |
|
|
Term
| 141. What species of Isospora infect dogs, cats, pigs, humans? |
|
Definition
Isospora spp.
dogs and cats
Cystoisospora spp.
several species
SI, LI, Ce
pigs
only 1 – Isospora suis
SI
humans
Isospora belli, I. natalensis
AIDS patients – severe |
|
|
Term
| 142. What host species does Eimeria infect? |
|
Definition
Eimeria spp.
birds
cattle, small ruminants
several species, few cause severe disease
horses
only 1 – Eimeria leukarti
rabbits, rodents
pigs |
|
|
Term
| 143. What developmental stages Eimeria and Isospora undergo? |
|
Definition
Eimeria spp.
birds
cattle, small ruminants
several species, few cause severe disease
horses
only 1 – Eimeria leukarti
rabbits, rodents
pigs |
|
|
Term
| 144. What symptoms does Isospora cause and is it zoonotic? |
|
Definition
Pathogenicity
occasional cause of diarrhea & death
enteritis, colitis, weight loss, dehydration
not zoonotic |
|
|
Term
| 145. What is a way to diagnose Isospora? |
|
Definition
history, clinical signs
fecal flotation, oocyst recovery |
|
|
Term
| 146. What are ways to control and treat Isospora? |
|
Definition
Control
kennel sanitation, prompt feces removal
sporulated oocysts can survive months in environment
disinfectants with high ammonia concentrations
resistant to most common disinfectants
Treatment
Sulfadimethoxine
only approved drug for enteritis associated with coccidiosis
Amprolium (not FDA approved)
Ponazuril appears effective (research) |
|
|
Term
| 147. What are characteristics of Cryptosporidium? |
|
Definition
Intestine
microvillus border
intracellular/extracytoplasmic
Thick and thin walled oocysts
small ≥ 4.5 um
Life cycle
asexual multiplication (sporogony/schizogony)
sexual reproduction (gametogony) |
|
|
Term
| 148. What stages of development does Cryptosporidium undergo? |
|
Definition
Phylum Apicomplexa
oocyst
sporozoite
trophozoite
schizont
type I
type II
merozoite
microgametocyte
macrogametocyte |
|
|
Term
| 149. What are transmission pathways for Crypto? |
|
Definition
direct contact with infective oocyst (in feces)
mucosal scrapings or tissue homogenates (from infected organs)
contaminated food or equipment, hands, shoes/boots or clothing of animal caregivers
water
Factors that increase risk of waterborne outbreak
close association between animals & humans
large numbers oocysts excreted (107 per gram of feces)
low infective dose
small oocyst size and oocyst resistance |
|
|
Term
| 150. How resistant are Crypto oocysts? |
|
Definition
Physical disinfection
heat to 64-72.4°C 1-5 min.
freezing down to -20°C
-70°C no survival
UV irradiation
high doses render oocysts noninfectious
Chemical disinfection
chlorine*
hypochlorite*
hydrogen peroxide
95-98% reduction 10-30 minutes
iodine
56-85% reduction 30-60 minutes
Doesn’t work
ethanol, isopropanol, Lysol, Pine-Sol, formaldehyde, betadine |
|
|
Term
| 151. What patients are most predisposed to get Crypto? |
|
Definition
Immunocompromised hosts – highest risk
AIDS/HIV-positive, ongoing chemotherapy, organ transplant
>2 L feces per day
“cholera-like”
frequently chronic
high rate morbidity & mortality |
|
|
Term
| 152. What are clinical signs of Crypto? |
|
Definition
most infections subclinical
profuse watery diarrhea
anorexia, dehydration, weight loss
villous atrophy, enteritis, fusion of villi (biopsy)
healthy dogs/cats – infections usually self limiting
persistent infections denote underlying cause such as canine distemper |
|
|
Term
| 153. How can we diagnose Crypto? |
|
Definition
oocysts in feces
fecal flotation – oocysts just right under coverslip
acid fast stain
H&E stain
ELISA, IFA
biopsy |
|
|
Term
| 154. Tx of Crypto in Animals and Humans? |
|
Definition
Animals
NO FDA approved treatment
Some efficacy:
paromoycin
tylosin
azithromycin
Humans
Nitazoxanide (Alinia™, Romark Laboratories)
synthetic compound has activity against many protozoans
interferes with anaerobic respiration |
|
|
Term
| 155. What are main characteristics of Toxoplasma gondii? |
|
Definition
Toxoplasma gondii
obligate, intracellular parasite
Hosts
Intermediate: most mammals
Definitive: members of Felidae family
mainly domestic cats
Transmission
Acquired
ingesting infective oocysts (feces, contaminated food/water)
consumption of raw/undercooked meat
Congenital
transplacental |
|
|
Term
| 156. What are Tachyzoites in Toxoplasma infection? |
|
Definition
| They are little things that can be extracellular or intracellular: Rapidly dividing – found in liver, lungs, spleen, lymph nodes |
|
|
Term
| 157. What are Bradyzoites in Toxoplasma infection? |
|
Definition
| Slowly dividing – found in brain, heart, skeletal muscle, eye |
|
|
Term
| 158. Life cycle of Toxoplasma gondii: |
|
Definition
Cat : ingests 1) sporulated oocyst
2) tachyzoite – congenital
3) bradyzoite – IH
Schizogony + Gametogony (in intestine);;
oocysts in feces;;
OOOOO>
IH: ingests 1) sporulated oocyst
2) tachyzoite – congenital
3) bradyzoite – IH;;
Tachyzoites develop in any cell except RBC;;
Immunity develops - Bradyzoites develop as cysts in host tissue
**cycle may reinitiate after decline of immunity cycle |
|
|
Term
| 159. Again, Toxoplasma gondii lifecycle? |
|
Definition
Lifecycle: Definitive Host
Prepatent: ingesting tissue cyst (bradyzoite) – 3-10 days
ingesting sporulatedoocyst – >18 days
ingesting tachyzoites – varies
Oocysts: 10x12um; sporulate 1-5 days
Patent period varies: 7-20 days
**can shed > 1 million oocysts/gram
Lifecycle: Intermediate Host
Tachyzoites develop after 12hr PI
Bradyzoites& tissue cysts develop by 6 days PI |
|
|
Term
| 160. Do clinically ill cats shed Toxoplasma oocysts? |
|
Definition
seroconvert 2-3 wks PI; most sero+ cats already shed oocysts
studies indicate cats shed once/lifetime unless re-infected
relapse shedding
concomitant infections w/ I. felis
immunosuppressionw/ high dose corticosteroids – but not FIV
not well understood |
|
|
Term
| 161. What are clinical signs in cats ill with Toxoplasma? |
|
Definition
| fever, anorexia, jaundice, abdominal pain/discomfort, hepatitis, pancreatitis, neurological problems, respiratory interference, death |
|
|
Term
| 162. Do dogs get infected with Toxoplasma gondii? |
|
Definition
Worldwide surveys
sero+ dogs
cross reaction w/ Neospora caninum ??
ongoing research |
|
|
Term
| 163. How can we diagnose Toxoplasma gondii? |
|
Definition
Fecal flotation (oocysts) – DH only
oocysts 10x12 um
Multiple serological examination (IFA, ELISA)
**one positive serum sample only indicates past infection
**16-fold rise in titer in serum taken 2-4 wks after 1st indicates acute acquired infection
Histological examination (biopsy)
PCR |
|
|
Term
| 164.Tx of Toxoplasma gondii? |
|
Definition
Cats
sulfadiazine & pyrimethamine
clindamycin hydrochloride/ clindamycin phosphate
Humans & Other Intermediate Hosts
sulfadiazine, sulfamethazine
pyrimethamine
clindamycin (pregnant women) |
|
|
Term
| 165. How to best control Toxoplasma infections? |
|
Definition
Cats
do not feed raw meat
keep cats indoors to prevent hunting
Humans
cook meat thoroughly
change litter box daily (avoid oocystsporulation)
wear gloves while gardening
Other intermediate hosts
remove dead animals or aborted fetuses promptly to avoid cannibalism
limit cat access to avoid water/food contamination w/oocysts |
|
|
Term
| 166. What are general characteristics of Neospora caninum? |
|
Definition
Hosts
Intermediate: cattle, sheep, goats, deer
Definitive: mainly dogs & coyotes
Worldwide distribution
Transmission
Acquired
ingesting infective oocysts (contact w/feces)
consumption of raw infected meat, aborted fetus, placenta
Congenital
transplacental |
|
|
Term
| 167.What are life stages of Neospora caninum? |
|
Definition
Bradyzoite
slowly dividing; tissue cyst
usually in CNS
can remain viable in tissue (dead animals) 7-10 days
Tachyzoite
rapidly dividing; any tissue
Oocyst
sporulates within 24 hours – infective stage
Prepatent period: (dogs) approx. 5 days
Patent period: varies, can be months |
|
|
Term
| 168. What patients have the worst infections with Neosporosis? |
|
Definition
Neosporosis most severe in congenitally infected puppies
limb paralysis – hind limb hyperextension “hallmark”
3-6 weeks after birth
not all littermates affected equally or simultaneously
Generalized disease some pups, older dogs
CNS involvement, myocarditis, hepatitis, pneumonia
If untreated, dogs with clinical neosporosis usually die & prognosis w/ treatment variable |
|
|
Term
| 169. How can we diagnose Neospora caninum? |
|
Definition
Fecal flotation (oocysts) – DH only
oocysts 11x11 um
Multiple serological examination (IFA, ELISA)
**rise in titer in serum taken 2-4 wks after 1st indicates acute acquired infection
**diagnosis in conjunction with clinical signs
titer ≥ 1:50 suggestive of infection
titer at least 1:200 – most dogs with clinical infection (but not always)
careful of cross-reactivity with Toxoplasma gondii
Histological examination (biopsy) - difficult
PCR |
|
|
Term
| 170. How can we treat Neospora caninum? |
|
Definition
Variable prognosis with treatment
better with adult dogs
Clinical improvement unlikely if rapidly ascending paralysis present
adults/older puppies: trimethoprim sulfadiazine &pyrimethamine or clindamycin
puppies 9-13 wks: clindamycin (dosage varies with age) |
|
|
Term
| 171. How can we control Neospora caninum infection? |
|
Definition
Limit canine exposure to animal housing facilities
limit oocyst contamination of food/water
Remove dead animals or aborted fetuses
prevent ingestion of infected meat
Do not breed bitches infected with N. caninum
Do not breed pups from infected bitches
Do not feed dogs raw meat
Zoonotic potential unknown |
|
|
Term
| 172. What phylum do Hammonida species belong to and what is their life cycle? |
|
Definition
Phylum Apicomplexa
Morphologically similar to Neospora and Toxoplasma
Obligatory 2 host lifecycle
Transmission
DH: ingest bradyzoites
IH: ingest oocysts
Primary species
Hammondia hammondi
Hammondia heydorni |
|
|
Term
| 173. Describe host and pathogenesis of Hammonida hammonidii? |
|
Definition
Hosts:
DH: cats
IH: rodents
Non-pathogenic |
|
|
Term
| 174. Describe the host and pathogenicity of Hammonida heydornai? |
|
Definition
Hosts:
DH: dogs, coyotes
IH: (known) cattle, water buffalo, camels, sheep, moose, goats
Associated with diarrhea |
|
|
Term
| 175. What is Hummonda life cycle? |
|
Definition
Lifecycle
No congenital transmission
DH: ingest bradyzoites
no extraintestinal stages – no tachyzoites, no cysts
schizogony and gametogony in intestine
prepatent period approx. 7 days
oocysts sporulate outside DH: 11x12um
IH: ingest oocysts
tachyzoites and bradyzoite cysts in skeletal muscle, lungs, lymph nodes, occasionally brain |
|
|
Term
| 176. How can we diagnose Hummonida? |
|
Definition
Neospora, Toxoplasma & Hammondia morphologically identical
Fecal Flotation
cat – Toxoplasma or H. hammondi
dog – Neospora or H. heydorni
Hammondia spp. are rare
Experimental PCR
Serology for Neospora & Toxoplasma
cross-reactivity ???
use with clinical signs and history |
|
|
Term
| 177. Sarcocystis main characteristics? |
|
Definition
Phylum Apicomplexa
Distribution - worldwide
Hosts
Predator – Prey Relationship
Definitive host: Carnivore
Intermediate host: Herbivore
Transmission
DH: consuming IH tissue containing sarcocysts
IH: ingesting food contaminated with sporocysts (DH fecal material) |
|
|
Term
| 178. What is life cycle of sarcosystis? |
|
Definition
Life cycle (heteroxenous)
DH: carnivore or omnivore
IH: herbivore
Definitive host passes oocysts/sporocysts
gametogony
Intermediate host produces sarcocysts (tissue cysts)
schizogony
the stage that may cause damage |
|
|
Term
| 179. Where does Gametogony occur in Sarcosystis? |
|
Definition
| Gametogony occurs in the intestine of the DH – bradyzoites penetrate lamina propria |
|
|
Term
| 180. Where are Sarcosystis sporozoites released from? |
|
Definition
| Sporozoites released in intestine & invade many tissues – Schizonts form in endothelial cells of blood vessels of brain, liver, kidney – sarcocysts form in skeletal and cardiac muscle of IH |
|
|
Term
| 181. How can we detect Sarcosystis spores? |
|
Definition
Fecal flotation
sporulated oocyst (DH)
cats (12-13 x 8-9 um)
dogs (12-16 x 10-11 um)
Biopsy or necropsy
schizonts in muscle or brain (IH) “rosettes”
sarcocysts
Western blot
Ab in serum or CSF
CSF only for S. neurona
PCR
History of presence of dogs/cats on premises |
|
|
Term
| 182. How can we control Sarcosystis infections? |
|
Definition
bury/incinerate dead livestock
cover stored grain
keep carnivores out of animal housing facilities |
|
|
Term
| 183. What are some common piroplasmids? |
|
Definition
Genera:
Cytauxzoon
Babesia
Theileria
Develop in erythrocytes
Indirect Life Cycles
ticks used as vectors
Diagnosis
blood smears
serology |
|
|
Term
| 184. What is Cytauxzoon felis? |
|
Definition
Phylum Apicomplexa
Order Piroplasmida – invasive stages ‘piroplasms’
intraerythrocytic
Emerging infectious disease in N. America
mainly southeastern & midwestern states
Hosts
DH: domestic cats
IH/vector: Dermacentor variabilis, Amblyomma americanum
Reservoir host: N. American bobcat |
|
|
Term
| 185. What is the Epidemiology of Cytauxzoon felis? |
|
Definition
Usually found in feral/farm cats
access to more ticks
Most often seen in summer
ticks in FL active longer
2008 Survey Bobcats
NC (C. felis recognized as problem in domestic cats)
30% surveyed bobcats + C. felis
PA (C. felis NOT recognized as problem)
7% surveyed bobcats + C. felis
Potential for disease present |
|
|
Term
| 186. Life cycle of Cyauxzoon felis? |
|
Definition
1. Tick feeds on infected host – ingests piroplasms (infective stages) in erythrocytes
2. Piroplasms develop into schizonts and travel to the salivary glands of the tick
3. Infected tick feeds on DH (cat) – schizogony occurs in macrophages
Merozoites released when macrophage ruptures – enter erythrocytes – develop into piroplasms
4. Transstadial transmission can occur – transmission from one life cycle stage to another |
|
|
Term
| 187. What is fatal form of Cytauxzoon felis infection characterized by? |
|
Definition
fever (up to 105°F)
depression
lethargy
anorexia
jaundice
death < 1 week |
|
|
Term
| 188. What is non-fatal form of Cytauxzoon felis infection characterized by? |
|
Definition
similar signs as ‘fatal’ form
also can be asymptomatic
persistent parasitemia |
|
|
Term
| 189. What stage of development of Cytauxzoon is most destructive and why? |
|
Definition
Schizogenous phase most destructive
macrophages infected w/schizonts block blood vessels
multi-organ failure
Clinical signs approx. 10 days PI
severe cases rapidly progressive; 6 days PI
Postmortem
dark, enlarged spleen
lungs, lymph nodes reddened and petechiated
pericardial sac may contain gelatinous, icteric fluid |
|
|
Term
| 190. How can we diagnose Cystauxzoon felis infection? |
|
Definition
Giemsa stained thin blood smears
piroplasms
PCR
biopsy/necropsy visceral organs
histiocytes – nucleus displaced, cytoplasm filled with granules |
|
|
Term
| 191. How can we control Cytauxzoon felis infection? |
|
Definition
keep cats indoors
use acaricides for tick control
promptly remove ticks from cats allowed outdoors |
|
|
Term
| 192. Is there any tx for Cytauxzoon felis infection? |
|
Definition
Supportive care
IV fluids
antimicrobials
heparin
Atovaquone & Azithromycin |
|
|
Term
| 193. What are the two most important species of Babesia? |
|
Definition
Phylum Apicomplexa
Invasive stages – PIROPLASMS
intraerythrocytic
apical complex, pear-shaped
Worldwide distribution
2 main species in dogs (U.S.)
Babesia canis
Babesia gibsoni |
|
|
Term
| 194. Describe Babesia canis? |
|
Definition
Vertebrate host
dogs, wolves, jackals
Arthropod host
Ixodid ticks – Rhipicephalus sanguineus or Dermacentor spp. |
|
|
Term
| 195. Describe Babesia gibsoni? |
|
Definition
Vertebrate host
canids
Arthropod host
suspect Rhipicephalus sanguineus in U.S. (if by tick) |
|
|
Term
| 196. Effects of Babesia canis on adults, puppies, transmission? |
|
Definition
Adults
usually carriers
mild/unapparent disease
Puppies
severe disease
Transmission
ticks main vectors |
|
|
Term
| 197. Effects of Babesia gibsoni on adults, puppies, trasnsmission? |
|
Definition
Adults & puppies
same disease, any age
History
Introduced to US in 70s-80s via Bull Terriers
Endemic in Africa, Middle East, Asia
Transmission (in U.S.)
fighting, ear cropping, tail docking, blood transfusions, transplacentally |
|
|
Term
| 198. Describe clinical signs of Babesia infection? |
|
Definition
Acute or Chronic
erythrocyte destruction and anemia
Clinical signs
anemia, pale mucous membranes, fever, amber/brown urine, splenomegaly
thrombocytopenia
B. canis: mild to severe
B. gibsoni: can be severe and persistent |
|
|
Term
| 199. How can we diagnose Babesia? |
|
Definition
Blood film
piroplasms visible only if clinically ill – not if carrier
detection 1 week PI; parasitemia peaks 3-4 wks PI
IFA
problematic; false negatives/positives
titers >1:80 significant; most 1:320
cross reactivity
PCR
will detect carriers
differentiate between species |
|
|
Term
| 200. How can we treat Babesia canis? |
|
Definition
Mild anemia – not therapy required
can be reservoirs
Relapse possible
Carriers – treated or not
Imidocarb dipropionate (Imizol) |
|
|
Term
| 201. How can we treat Babesia gibsoni? |
|
Definition
Combo treatment
Azithromycin & Atovaquone
Supportive care
blood
fluids
Relapse more likely
Does not respond as well to imidocarb dipropionate |
|
|
Term
| 202. What are two main arthropod classes to know? |
|
Definition
Phylum Arthropoda
Class Insecta
six legs, head – thorax – abdomen
Class Arachnida
eight legs (adults); six legs (larva)
head – body |
|
|
Term
| 203. Phylum Arthropoda-class Insecta? |
|
Definition
segmented body
head (brain, antennae, mouthparts, eyes)
chewing (grasshopper)
piercing/sucking (Reduviid bug, mosquito)
lapping (bee)
siphoning (butterfly)
sponging (housefly)
thorax (legs, wings)
abdomen (reproductive organs) |
|
|
Term
| 204. What is siple metamorphosis? |
|
Definition
| All stages look the same, only get bigger progressively. |
|
|
Term
| 205. Complex (complete) metamorphosis? |
|
Definition
| Is when all stages look different |
|
|
Term
| 206. What is class Arachnida? |
|
Definition
Phylum Arthropoda – Class Arachnida
Order Acarina
2 body regions
head (gnathosoma/capitulum)
body (idiosoma)
most: fused cephalothorax & abdomen
Simple (incomplete) metamorphosis
larval/nymphal stages not sexually mature |
|
|
Term
| 207. What are characteristics of order Diptera? |
|
Definition
1 pair of wings
second pair – vestigial halteres
Ectoparasites
permanent (entire life cycle)
temporary
attack for blood meal (usually females, some males)
Disease vectors
viruses, bacteria, rickettsiae
Intermediate hosts
protozoan & filarial parasites
Myiasis
larval stages develop in living tissue |
|
|
Term
| 208. What is facultative and obligatory myiasis? |
|
Definition
Dipteran larvae develop in living tissue
Facultative Myiasis
-Dipteran larvae normally free-living
-Can use living tissue OR carcasses
Obligatory Myiasis
-Dependent upon animal host for completion of life cycle |
|
|
Term
| 209. Describe Facultative Myiasis? |
|
Definition
NORMALLY eggs deposited in:
garbage, feces, rotten carrion
OCCASIONALLY eggs deposited in:
contaminated wounds
Larval ID:
spiracular plates “fingerprints” unique to each genus – 3rd stage instar
Early lesions:
dermatitis, numerous maggots, pungent odor, inflammation |
|
|
Term
| 210. Do Blow Flies use Facultative myiasis? |
|
Definition
Hosts: any mammal
Metallic hue
black, blue, green, orange
Vomit-drop feeders
Complex metamorphosis
dead, spoiled tissue, carrion, garbage
neglected, purulent wound
YES |
|
|
Term
| 211. Pathogenesis of Facultative myiasis? |
|
Definition
Pathogenesis
cutaneous myiasis (sheep)
Wound strike, Fly strike, Fleece Rot
toxemia, death
Diagnosis
dermatitis, pungent odor
larval ID
Treatment
remove larvae – watch for newly hatching larvae
treat secondary bacterial/fungal infections |
|
|
Term
| 212. Describe Obligatory myiasis? |
|
Definition
Larvae MUST use animal host to complete life cycle
Living tissue
Organs
Uncontaminated wounds
Soft tissue
-nose, navel, anus
Larval ID:
spiracular plates “fingerprints” unique to each genus – 3rd stage instar |
|
|
Term
| 213. Example of Obligatory myiasis is a Screwworm (Cochliomyia hominivorax). |
|
Definition
Primary Screwworm”
Eradicated by sterile male release (1950s)
US, Mexico, Central America, Panama
REPORTABLE (APHIS)
Identified by trachea of 3rd stage larva
deeply pigmented, dorsal posterior
2 dark stripes ⅓ body length
Affects any mammal
Fresh, recent wounds, living tissue
Breeds only once during life time
can lay up to 2800 eggs
larva emerge in 24 hours
First fly on the scene ( 1° screwworm) |
|
|
Term
| 214. Pathogenesis , diagnosis and treatment of screwworms? |
|
Definition
Pathogenesis
toxemia, bacterial infections
death
Diagnosis
larval ID
dermatitis, pungent odor
Treatment
remove larvae, watch for newly hatching larvae
treat secondary bacterial/fungal infections |
|
|
Term
| 215. What species use Obligatory myiasis? |
|
Definition
Cuterebra: Wolves”, “Warbles”
Hosts: cats, dogs, rabbits, rodents
Adults
large bodied
“bumble-bee” like
shiny, black abdomen
non-parasitic
Larvae
large
covered with spines
darken with maturity |
|
|
Term
| 216. Life cycle of cuterebra? |
|
Definition
eggs deposited near entrance to burrow/nest (rabbit or rodent)
larvae attach to host as pass by
larvae burrow into skin
subcutaneous cysts produced
maturation – 1 month
pupate in soil
adults emerge in Spring
cats and dogs infested by chasing rabbit/rodent into burrow
usually on face or neck |
|
|
Term
| 217. Pathogenesis, diagnosis, and tx of Cuterebra? |
|
Definition
Pathogenesis
cysts and swellings – secondary infections
larval migrations (esp. dogs/cats)
Diagnosis
larval ID
Treatment
surgically remove larvae |
|
|
Term
|
Definition
Anoplura and Mallophaga::
Pediculosis
infestation of lice
Veterinary importance
irritation to host
severe infestation can cause anemia
social stigma (humans)
disease vectors::
Small, wingless
1-5mm
Dorsoventrally flattened
Claw/crab-like legs
Permanent ectoparasite
Stenoxenous
very host specific
Simple metamorphosis
egg/nymph/adult |
|
|
Term
| 219. What are lifecycle characteristics of Anoplura and Mallophaga? |
|
Definition
Females produce 1 egg (nit) at a time – cemented to hair shaft or feather
50-100 eggs/female
Egg (nit) hatches 1-3 weeks – 3 nymphal stages
Adults within 4 ½ weeks |
|
|
Term
| 220. What can a shape of Mallophagia's head tell you? |
|
Definition
Looks like an M (stout), can't really bite, so does not suck blood.
Chewing/Biting Lice
skin scurf, epithelial cells
Head wider than thorax |
|
|
Term
| 221. What can a shape of Anoplura's head tell you? |
|
Definition
Sucking Lice
blood feeders
Head (cone-shaped) narrower than thorax |
|
|
Term
| 222. Describe order Sephanoptera? |
|
Definition
Siphonapterosis
infestation with fleas
2000 species
95% on mammals
Powerful jumpers
40% veterinary effort
flea control and diseases
plague, tularemia, Dipylidium caninum, Hymenolepis nana, Dipetalonema reconditum
Laterally compressed
Wingless
Ctenidia (combs)
Complex metamorphosis
egg/larva/pupa/adult
adults on host, blood feeders
Irritation, restlessness, anemia, flea allergy dermatitis |
|
|
Term
| 223. Name several common species of fleas? |
|
Definition
Ctenocephalides felis
dog & cat
common
Ctenocephalides canis
dog & cat
rare
Pulex simulans
dog & cat
Xenopsylla cheopis
Oriental rat flea
Bubonic plague
Echidnophaga gallinacean
Stick-tight flea, Poultry flea
dog, cat, humans
Tunga penetrans
Jigger flea, Sand flea |
|
|
Term
| 224. Is majority of flea life cycle on or off the host? |
|
Definition
|
|
Term
|
Definition
Laid on host, quickly fall off
oval, 0.5mm
Hatch 2-16 days
50% hatch 1.5 days
70% RH; 95°F
≥ 500 eggs/female
some reports 27 eggs per day over 50 days (1350 eggs) |
|
|
Term
| 226. Describe flea larvae? |
|
Definition
Larval stage – 7-10 days
2 molts; 3 instars
covered in setae
found in crevices, rugs
feed on “frass”
feces, dried blood
darken after feeding
susceptible to heat and desiccation
cannot survive below 50% RH and > 95 F (longer than 40 hrs) |
|
|
Term
| 227. Describe flea pupae stage? |
|
Definition
Pupal stage – completed in 4 days
adults can emerge in 5 days
emergence can be prolonged up to 174 days
adult flea fully developed in 10-17 days
Larvae become coated in particles from environment
dirt, sand, debris |
|
|
Term
| 228. Describe flea adults? |
|
Definition
Mate once
female stores sperm in spermatheca
Begin feeding < 1 hour after colonizing host
blood consumption increases body weight by 140% |
|
|
Term
|
Definition
Flea Allergy Dermatitis:
Biting fleas introduce salivary proteins (antigens)
At least 15 different complete proteins present
Severity of FAD related to duration of feeding and amount of salivary protein introduced
Onset of FAD
Most commonly 3-5 years of age1
Geography of lesions
Lumbo-sacral region, caudal thighs, proximal tail, ventral abdomen
Characteristics of lesions
Papules, crusts, alopecia, excoriations, erythema, hyperpigmentation
Secondary infections |
|
|
Term
| 230. What is the term for flea stool? |
|
Definition
FRASS. Hair and “frass” obtained with
a fine-toothed flea comb |
|
|
Term
| 231. What is the best flea control protocol? |
|
Definition
Integrated Flea Control
Combination of chemical and mechanical means which target
both the animal and its environment
Host-targeted insecticides
Insect Growth Regulators (IGRs) and Insect Development Inhibitors (IDIs)
disrupt egg and larval development
Adulticides
**repeated bathing can decrease efficacy of some topicals |
|
|
Term
| 232. How to use combination of chemical and mecanical flea control? |
|
Definition
Environmental insecticides
target areas visited by animals and wildlife
Ignore open sun-lit areas, use target sprays (particularly IGRs)
in areas where pet spend most of their time
Mechanical methods
Indoors: vacuum, wash pet bedding
Outdoors: remove vegetation, litter, prevent wildlife entry in crawl spaces, under decks, etc. |
|
|
Term
| 233. Issues important in flea control? |
|
Definition
client compliance
pupal window (adult quiescence)
performance of adulticides
microenvironments and flea infestations
client perceptions
insecticide resistance |
|
|
Term
| 234. Main characteristics of ticks and mites? |
|
Definition
Order Acarina
ticks and mites
Acariasis
infestation by mites or ticks
Otoacariasis: infestation of auditory ear canal
Intermediate hosts, vectors |
|
|
Term
| 235. Characteristics of ticks only? |
|
Definition
Characteristics of ticks
over 800 species worldwide; 60-70 in US
all stages, male and female feed on blood
2 Families
Ixodidae – hard ticks
Argasidae – soft ticks
Simple metamorphosis
1-Host, 2-Host, 3-Host tick lifecycles |
|
|
Term
| 236. What is tick paralysis? |
|
Definition
Ascending, flaccid paralysis
neurotoxin in tick saliva
disrupts nerve synapses in spinal cord
blocks neuromuscular junctions
Reversed with tick removal
can cause death
Feeding female
over 40 tick species
1st signs 5 days after attachment |
|
|
Term
| 237. What are basic body divisions of ticks? |
|
Definition
Basic body division
Capitulum (head)
mouthparts
toothed hypostome
basis capituli
Idiosoma (fused cephalothorax & abdomen)
scutum: ornate vs. inornate
male v. female
festoons
8 legs: adults, nymphs 6 legs: larvae |
|
|
Term
| 238. What is tick life cycle? |
|
Definition
1. Entire Lifecycle 6 weeks to 3 years
2. Engorged female deposits eggs on ground (100-18k)
3. Larva – seed tick – 6 legs
4. Nymph – 6 legs – sexually immature |
|
|
Term
| 239. What two modes of disease transmission are used by ticks? |
|
Definition
Disease Transmission
Transstadial transmission
disease/pathogen acquired during one life stage stays with the tick and can be passed in another
Ex: picked up as seed tick, transmitted to another host as nymph or adult
Transovarial transmission
disease/pathogen passed from female to developing offspring
Ex: deposited eggs are infected and transmission can occur as larvae |
|
|
Term
| 240. Soft ticks (Argasidae)? |
|
Definition
soft tick
lack scutum
periodic parasite
--feed quickly, do not engorge, leave host
mate off host
mouthparts NOT visible |
|
|
Term
| 241. Hard ticks (Izodidae)? |
|
Definition
hard tick
possess scutum
permanent parasite
--can remain on host for days
females engorge
mouthparts visible |
|
|
Term
| 242. Describe Ripicephalis sanguineus (Brown dog tick)? |
|
Definition
“Brown Dog Tick”
inornate scutum
Three host tick
mainly dogs (all 3 stages)
common on ears, between toes
Throughout US
Tick paralysis
Disease vector
Hepatazoon canis
Babesia canis
Ehrlichia canis |
|
|
Term
| 243. Describe Ixodes scapularis? |
|
Definition
Black legged tick”
inornate scutum
Three host tick
birds, small mammals
cattle, sheep, horses
Southeastern to S. Central US, along East Coast
Disease vector
Borrelia burgdorferi (Lyme)
Babesia microti
Anaplasma marginale |
|
|
Term
| 244. Describe Amblyomma Americanum? |
|
Definition
Lone star tick”
white spot on female scutum
Three host tick
rodents, rabbits
deer, cattle, horses, sheep
Tick paralysis
Southern US
early spring to late summer
Disease vector
Rickettsia rickettsii (RMSF)
Borrelia burgdorferi (Lyme)
Francisella tularensis (tularaemia) |
|
|
Term
| 245. Dermacentor variabilis tick? |
|
Definition
“American dog tick”, “wood tick”
ornate scutum
Three host tick
rodents, small mammals
dog (preferred), cow
Most of US
Tick paralysis
Disease vector
Rickettsia rickettsii (RMSF)
Anaplasma marginale |
|
|
Term
|
Definition
Microscopic or barely visible
Pedicels (legs/stalks) – ID
suckers present/absent
short vs. long
jointed vs. non-jointed
Surface dweller or tunnel through skin layers
larva – 6 legs; adult – 8 legs
2 body divisions:
head– gnathsoma
body – idiosoma |
|
|
Term
| 247. What are Otodectes cynotis? |
|
Definition
“Ear mite”
Host: dogs, cats, foxes, raccoons, ferrets
In external ear canal
surface dwelling
Short, nonjointed pedicels
females: suckers leg pairs 1, 2, 4
males: suckers on all leg pairs
Permanent parasite |
|
|
Term
| 248. How can animal get Otodectis cynotis and what are clinical signs? |
|
Definition
Direct contact
Clinical signs
thick, tarry exudate within external ear canal
host shakes head, scratches ears
infections of middle/inner ear can develop if untreated |
|
|
Term
| 249. How can we diagnose and tx Otodeces cynotis? |
|
Definition
Diagnosis
swab external ear canal – look for mites
Treatment – limited residual action – regular application at least 10 days
thiabendazole
monosulfiram
permethrin |
|
|
Term
| 250. What is Demodex canis? |
|
Definition
“Follicle mite of dogs”
Host: dogs
In hair follicles & adjacent sebaceous glands
Alligator/cigar shaped
adults – 8 legs
larva – 6 legs
Permanent parasite |
|
|
Term
| 251. What are the signs of localized vs. generalized Demodex infection? |
|
Definition
Localized
skin redness
partial hair loss
usually no itching
commonly on face, around eyes
oooo>
Generalized
more severe
large patches of alopecia
secondary bacterial infections
pyoderma |
|
|
Term
| 252. How can Demodex be transmitted and how we can diagnose ant tx it? |
|
Definition
Direct contact
usually mother to offspring
Diagnosis
deep skin scraping (follicle)
pustule & abscess contents
Treatments
localized – usually resolves spontaneously
generalized – amitraz dip (250 ppm every 2 wks)
not approved treatments for demodecosis – ivermectin, oral milbemycin oxime, topical moxidectin
Not zoonotic |
|
|
Term
| 253. What is Cheyletiella? |
|
Definition
“Walking dandruff”
Hosts: dogs and cats
may set up temporary residence on humans
Found in fur coat, keratin layer of dermis
Surface dwelling, non burrowing
ID: bell-pepper shaped, 500 um
mouthparts resemble hooks/horns |
|
|
Term
| 254. What are clinical signs, diagnosis and tx of Cheyletiella? |
|
Definition
Clinical signs
asymptomatic
severe – dandruff, itchiness, reddened skin, hair loss
Diagnosis
microscope
mites on skin, in fur/hair
skin scrapings not necessary
Treatment
easily killed, most flea shampoos will suffice |
|
|
Term
| 255. What is Pneumonyssoides caninum? |
|
Definition
“Nasal Mite”
Hosts: dogs, other caninds
Direct Contact
Nasal passages and sinuses
ID: oval, creamy white, legs anterior half of abdomen
females: 700-1500um |
|
|
Term
| 256. Clinical signs, diagnosis, and tx of Pneumonyssoides caninum? |
|
Definition
Clinical signs
usually asymptomatic (non pathogenic)
reddening of mucosa, sneezing, head shaking, rubbing nose
Diagnosis
microscopic ID
Treatment
ivermectin (not approved) |
|
|
Term
| 257. What is Notoedres cati? |
|
Definition
“Notoedric acariasis mite”
Hosts: cats, rabbits
zoonotic
Mainly ears, back of neck
females: burrow/tunnel in epidermis
males/larvae/nymphs: skin surface, near tunnel openings
ID: round body, long nonjointed pedicels
females: suckers leg pairs 1 & 2
males: suckers leg pairs 1, 2 & 4 |
|
|
Term
| 258. What are clinical signs, diagnosis, and treatment of Notoedres cati? |
|
Definition
Clinical signs
persistent pruritus, alopecia
yellow crusts (face/neck)
Diagnosis
deep skin scrapings
microscopic ID
Treatment
selamectin (Revolution®) |
|
|
Term
| 259. What is Sarcoptes scabei? |
|
Definition
“Sarcoptic acariasis mite”, “itch mite”
Hosts: dogs, cattle, horses, sheep, goats, swine (rarely cats)
zoonotic
Direct contact – highly transmissible
Dogs – muzzle, eyes, ears
females: burrow/tunnel in epidermis
males/larvae/nymphs: skin surface, near tunnel openings |
|
|
Term
| 260. What are clinical signs of Sarcoptes scabei? |
|
Definition
Clinical signs
irritation, itching, exudate forms crusts
thickening of skin, alopecia
severe cases result in death (large lesions) |
|
|
Term
| 261. What is a way to diagnose Sarcoptes scabei? |
|
Definition
Diagnosis
Deep skin scrapings
ID: gray-white, barely visible, long nonjointed pedicels
females: 400-500 um, suckers leg pairs 1 & 2
males: 200-250 um, suckers leg pairs 1, 2, & 4 |
|
|
Term
| 262. What is a way to treat Sarcoptes scabei? |
|
Definition
Treatment
Treat all in-contact animals
5% permethrin, benzyl benzoate
antibiotics (2° infections)
hydrocortisone creams |
|
|
