Week 1 Flashcards
Significance of ascarids (common roundworms- mostly SI)
Mammals, birds, other
* commonly usually young hosts <1 year unless immuno suppressed
* old animals can represent reservoirs
* Usually host and site specific (adults; mostly SI); other sites (larvae**)
* Some are zoonotic; can use paratenic/ transport hosts (e.g. earthworms)
* Production losses and clinical disease
Usually large adults 5-15 cm
Females and males (males 2 spicules)
Three lips
Some have alae (wings) and or bulbus
* oviparus- lay formed eggs without larvae in them
* All ascarids need the eggs to mature in the environment for them to be infective
Ascaris (thick-shelled) eggs (sticky)
Bottom egg has L3 and is infective to the host (once ingested parasite can migrate)
* Ascaris suum
* Direct LC
PPP=months
* females lay hundreds of thousands of eggs everyday
* Hepatopulmonary migration
* Can be transported by earthworms, but no development occurs in the earthworm.
* eggs are ingested–> eggs are pretreated in the stomach- loosens up the shell–> SI–> change in pH activates the larvae to come out–> transported passively in the blood stream to the liver–> migration in the liver about 5 days (move quick due to immune response is rapid in the liver)–> eventually up the trachea–> swallowed–> L4 ends up in stomach–> SI and establishes
Ascaris suum
* alpha-pepsin and alpha-trypsin enzymes
* maldigestion and malabsorption
* impaction can occur
* can sometimes perforate SI but rare
Hepatitis parasitaria multiplex of Ascaris suum
* Mechanical damage and eosinophilic inflammation > fibrosis (repair) > regeneration
* Ascaris suum
Mechanical damage to lungs as well, haemorrhage and eosinophilic inflammation (IgE/ histamine)–> rapid, shallow breathing with coughing; secondary infections (atypical host> anaphylactic response)
Effects and consequences of Ascaris suum
Parascariasis (impaction in horses)
Parascaris equorum
Parascaris equorum (Ascarid)
Ascarids of canids and felids
* Toxocara canis- also has transplacenta transmission, can have transmammary as well, oral, and hepatopulmonary
* Toxocara cati- transmammary or transcolostral transmission, oral, hepatopulmonary
* Toxascaris leonina- oral, intestinal wall
which one is which?
Toxocara canis LC
Young animal < 3 months–> oral infection route if not previously infected–> HP migration–> establishes in SI
* After 3 months dogs become more resistant. The parasite tends to be blocked from migration. Does not migrate up the trachea anymore.
** rodents MAY play a role- they carry L3s or premature L4s– larval establish directly in the gut
** Can undergo arrested development- sequester away in the muscle tissues and WAIT– no significance in the male dog because they don’t go anywhere.. but the female dog this plays a huge role in transmission (last 1/3rd of pregnancy- larvae become activated- come out of arrested state- migrate to the placenta via the umbilical cord get into the foetus in utero- undergo hepatopulmonary migration in the foetus)
** when eggs are excreted from the dog they are not directly infective, it takes 2-3 weeks of development
** zoonotic, cause ocular granulomas
** Larvae are not fussy, but Toxocara canis only want the SI of a canid host**
PPP of oral route= 4 weeks
PPP in puppy= 2-3 weeks
Canine toxocariasis
Canine toxocariasis
Toxascaris leonina LC
No HP migration, it does migrate in the intestinal wall, oral transmission
Toxocara vitulorum
Young animals infected orally BUT the main way it passes on to offspring is via milk
* Mainly in the tropics
Control “equation” general
Control of ascarids general considerations
* Prolific egg layers (heavy contamination)
* hygiene (host and environment)
* most disinfectants have no nematocidal effect
* young animals usually develop good immunity
* Some species are zoonotic
* Direct LC: oral transmission, migratory routes: HP, TP, TM, S, M > changes PPP
* Differential drug efficacy (adult vs. larval stage)
PPP in months? Migration?
Differential drug efficacy of ascarids
What anthelmintic resistance is important with adults (SI) ascarids?
What drugs should be used against ascarid larvae?
Heterakis isolonche (pheasant)
Name the ascarids that impact birds
What is an ascarid that has an indirect life cycle?
humans ingest by eating sushi that has not been frozen first
Oxyuris equi (pinworm)
female worm lays eggs at night, in egg packets (stick substance attaches eggs together)
* Use sticky tape to diagnose
* it is itchy- why horses get the scraggly tail
* control- common nematocides (unknown how effective)- although non-pathogenic, very diffcult to control- key is to clean environment to rid of contamination (saddles, bridles, etc.)– also rotate drugs. Unknown if inefficacy or just resistance.
* > 1 year of age, they do develop good immunity- you might see it later if immunosuppressed
* Transmission from grooming or just contact with other infected horses
General info on spiruroids
* Not in the SI or LI (like ascarids and oxyurids)
* unique outer features
* you will only see them in feral or free range animals, wild carnivores, free range chooks, not in domesticated animals
* Not easy to control because they all have indirect life cycles- rely on arthropods as intermediate hosts
Significance of spiruroids
* generally induce a chronic infection- get into nodules
* when they get in they induce a granulomatous type lesion
* many are upper alimentary tract; some in skin/eye
* distribution: northern or central Australia; some are rare
* INTERMEDIATE HOSTS
* some of human health significance
Spiruroids
Dracunculus medinesnsis (spiruroid; Middle East & India)
Female: ~100 cm; male ~50 cm. Via copepod in drinking water (L3)
* used stockings to filter drinking water
Spiruroids
* Developed buccal capsule and cuticular structures
* Muscular and glandular parts of the oesophagus
* Spicules unequal in length (male)
* Mostly ovo-viviparous (eggs containing L1)– meaning laying
* Indirect LCs (arthropods; L3 mostly ingested by host)
What spiruroids affect horses, dogs/cats, pigs, ruminants, birds?
(FARM (amphibians, reptiles, mammals))
Habronemiasis in horses
(spiruroids)
(spiruroid)
* can cause colic and death
Why is it difficult to diagnose habronema?
Due to low fecundity, hard to find an egg
Life cycle of Habronema (spiruroid)
Life cycle will only perpetuate if the adult can develop in the stomach
** can deposit larvae on moist skin
What is this? How do you control?
Granulomatous lesion from Habronema (spiruroid)
Hard to get rid of, hard to kill
Macrocyclic Lactones (Ivermectin) work against LARVAL stages, not ADULT stages.
Gastric form- Habronemiasis- this how it perpetuates when it establishes in the stomach
Cutaneous form of habronemiasis (spiruroid)
Larvae establishing in moist skin
this is NOT how it perpetuates the life cycle
Spiruroids in cats and dogs. What IH?
Spirocerca lupi
* dogs and cats (spiruroid)
* vomit- check pH- can tell you if there is a lesion in the URT– helps determine ddx’s
Life cycle of Spirocerca lupi
* pepsin activates them in the stomach–> migrate through vessels from the stomach into aorta–> after months undergo a moult, moult again as they get out of the aorta–> migrate around in the mediastinal tissues–> migrate down the oesophageal length to terminal part of the oesophagus where they start irritating the wall of the digestive tract
Spirocerca lupi (significant carcinogen)
Hyperplasia and inflammation, can lead to CANCER, very difficult to operate in the oesophagus (more success if in the stomach)… Cancer is METASTATIC (via the blood stream to other organs). Locally= fibrosarcoma OR fibrosteosarcoma (depending on how the cancer develops)
Spirocerca lupi (in a cat, could be pus filled)
Physaloptera praeputialis (via beetle; blood-feeder)
(dogs and cats; spiruroid)
Cylicospirura felineus
& C. subequalis (via arthropods)
CATS; spiruroid
Gnathostoma spinigerum
(cat; spiruroid)
Life cycle of Gnathostoma spinigerum
Cats; spiruroid
Cat ingesting fish with L3
Spiruroids in pigs
Gnathostoma hispidum
Physocephalus sexalatus
pigs; spiruroid
Spiruroids in ruminants
Thelazia species (eye-worm; viviparous)
ruminants; spiruroids
Thelazia callipaeda
Spiruroids in chickens
Why is control difficult for spiruroids?
Drugs have to be lipophilic in order to get into nodules and into the parasites to kill them
* the variety and abundance of intermediate hosts
* febendazole is quite good
** Macrocyclic lactones are lipophilic
General on filarioids
* Not in GI tract
* emphasis on heartworm
Transmitted by a tabanid fly
Mostly viviparous (only spiruroid that is viviparous is Thelazia)
* look for microfilaria (with heartworm) in the blood stream
Significance of filarioids
Large problem in developing nations
* Elephantiasis- chronic lesions- leading to problems with flow of lymph and blood leading to congestion
* Difficult to identify as they do not have unique morphologies.. therefore consider site specific and geography
What filarioids impacts humans, horses, cattle, dogs/cats?
Distribution of Wuchereria bancrofti, Brugia malayi, Onchocera volvulus
Loa loa (via tabanid)
Ivermectin isn’t as lipophilic as some other MLs
L3 penetrates the skin and migrate to the nuchal ligament. Establish, grow, and moult and develop into the adult stage (M/F). Nodules become granulomatous and cause problems in this area. The real problem is not just the nodules in the nuchal ligament, but it is the larval stages produced by the female which come out in surrounding tissues and migrate to the site of prediliction, where the culicoides will suck up when they feed. L1 stages are what migrate off…. and taken up…. L3 develops in the arthropod.
What are the filarioids in cattle?
Big problem in northern australia. In the brisket cutting out the lesions.
In the lesion it is one long female with males
Distribution of Onchocerca of cattle
Stephanofilaria (via buffalo fly)
* embedded in the skin
* Causes hair loss
Setaria labiatopapillosa (via mosquito; non-pathogenic)
Control of filarioids
Control: Difficult because of IH’s
Treatment: Humans/horses vs. livestock- do not tend to treat individual livestock
* Treatment against microfilarial stages (dermatitis or ocular diseases)– macrocyclic lactones
* Leads to production loss because they have to get rid of the nodules in meat
Distribution
Dirofilaria
Prevalence of Dirofilaria in Australia
Prevalence of the vector declines as you travel south in Australia. Where mossies do well, heartworm does well. With the use of preventive drugs, massive decline. Dingos and wild dogs are reservoirs for infecting mossies, continuing the cycle. Urban environment had a massive decline *infection pressure is low down south*
Life cycle of Dirofilaria immitis
*Primary host is canid but there is spillover (cats- not infection that gives rise to offspring “amicrofilaraemic”– so you don’t need to prevent cats from infecting mossies, humans)
*L3s depositing (not injecting!) on the skin, go through mossie bite into skin, under skin layers into the dermis–> migrate around–> 10 days (first moult) they moult to become L4–> after 70 days (second moult) moults to pre-adult–> after 3 months it travels to the heart via the bloodstream–> after 6 months (grown and have become reproductively active, mated, and producing L1 stages) after mating with a male–> offspring produced –> female produces L1s that are in bloodstream transported everywhere–> gives rise to mossie becoming infected where within the mossie L3 is developed
* Obligatory indirect- L1 will not develop into L3 unless it is in the mossie
Infection of Dirofilaria immitis?
Chronic infection of older dogs. It is not acute. It takes a long time for heartworm to manifest clinically- it takes years. 3-5 yo or older in which we see signs.
* Adult worms in the pulmonary artery can survive for 2 years
* Parasite tends to be in the pulmonary artery, not the heart itself, only when there are very large burdens will the burden extend into the right heart, atrium, and then the ventricle.
Signs of heartworm infection
* Wet cough
* Exercise intolerance
Steps in the pathogenesis of heartworm
* Irritating vessel wall of pulmonary artery
“coagula” collect around the worm and can even block vessels
* you will get turbulence in the blood flow
* thickening in the vessel walls–> decreased laminar blood flow–> more rigid/ less elastic–> more turbulence + increased pressure
* the only way for the fluid to get out is via the airways because thecirculation is compromised
Pathogenesis of Dirofilaria
Caval Syndrome
BP building up becomes too much to cope. BP in Caval vein–> congestion in circulation in the abdominal cavity–> build up of fluid in liver, spleen, kidney, intestines–> release of fluids into abdominal cavity (ascites)+/- hydrothorax–> eventually leads to chronic progressive insufficiency systemically because the heart cannot cope
Caval syndrome, Dirofilaria immitis
Caval Syndrome
Dirofilaria immitis
How is Dirofilaria immitis diagnosed?
* Clinical- x-ray or ultrasound
OR
* Direct Diagnosis:
- Blood smear: drop of blood, low sensitivity!
- Knott test- 1 ml blood> lyse>centrifuge>stain>examine- detects 1 microfilaria per mL
- Filter test- 1 ml blood> lyse>filter>stain>examine- detects 1 microfilaria per ml
(Knotts uses a centrifuge vs. filter test just filtering)
*** 10-65% of dogs- no circulating microfilariae- “occult infections” (immature, single-sex, or senile worms)…. single sex worms with single sex infection with no reproduction therefore no larvae. OR if immune system hammers the worms or if they don’t grow well– then they are immature. OR senile worms- old and no longer reproductively active… these sorts of infections with no L1s are “occult infections”
Differentiated between Dipetalonema reconditum and Dirofilaria immitis
Dipetalonema reconditum (non-pathogenic)
What do you use for immuno-diagnosis of Dirofilaria immitis?
Antigen- ELISA (Because antibody is low sensitivity and low specificity)
* Antigen-ELISA: Specificity 98% & Sensitivity: 75-95% (depends on how many worms present, once you get over 3 worms, sensitivity increases)
Eliminate or decrease the ability of the worm to infect the dog host (or cat). Maintaining drugs in circulation. (some drugs only kill at the moulting stages and some only kill the larvae)
* Macrocyclic lactones
“microfilaricidal”
* DEC has to be administered daily only acts at day 10 and day 70.
* Do not kill adults effectively e.g. Milbemycin oxime- 5 times in a short time frame- you will get some effect to kill adults
* endemic area like QLD put dog on very early, prior to 3 months of age because you want to kill the worms before they become adults
* if you treat a dog already infected with circulating L1s, you can elicit allergic response because preventive dose will mass kill- immune response is already primed. (Knotts or Filter test first, possibly antigen ELISA test to be sure)– if positive there are options.
* not really in utero infections because of mossie.
Curative treatment for Dirafilaria immitis
Radiography guidance to remove worms through jugular vein
* keep the dog restrained, rest the dog–> when the worms are killed- do not want worms into a vessel to cause blockage, we want worms to degrade slowly and slowly release antigens
* Drug: Melarsomine dihydrochloride- administer multiple times- start killing the worms (adults) and they are start degrading. You can kill the L1 microfilariae after the adults. 2.5 mg/kg intramuscularly; 24 hours apart; can be repeated.
** could use Carparsolate or Levamisole (not as effective)
** likely to have embolisms from the worms.
Prevention vs. Curative treatment
What are considerations when dealing with clients and cases?
