Parasitology NEM Flashcards
1
Q
Ascaridida features how large, what eat, special structures and the eggs
A
- Large creamy nematodes (5-15 cm)
- Female»_space; Male
- Lumen dwellers feeding on gut contents (usually SI) - relatively non-pathogenic
○ Unless in large numbers can lead to malnourishment - Three large lips (with sensory features)
- Some have cervical alae (‘wings’)
- Tail end of male coiled
- May have caudal papillae and prominent ‘projections’
- Females prolific egg layers (200,000 eggs/day)
- Eggs thick-shelled, highly resistant -> eggs can live up to 70 years -> high burden
○ Very sticky
2
Q
List the 10 steps in the lifecycle of ascards
A
1) Adult in large intestines -> gut feeding and mating
2) Lots of eggs within the faeces - unembryonated egg - highly resistant
3) 1-3 weeks for egg to become embryonated
4) Two ways
1. Some use paratenic host (L3) -> larval migration into tissues - hypobiosis
○ Paratenic host ingested by definitive host -> adult within intestines (
○ NO MORE MIGRATION
2. Some use definitive host (L3) -> small intestines
5) Larvae hatch enter circulation -> UNDERGO HEPATOPULMONARY MIGRATION
6) Into the liver -> afferent vessels of the liver -> penetrate -> efferent vessels
7) Blood stream -> pulmonary vessels -> stuck in lungs
8) Into alveolar space (destroy) -> tracheal migration
9) Coughed up and swallowed
10) Large intestines
3
Q
Ascarids significance how common, what age and why
A
- Common! Usually young hosts < 1 year
- Strong exposure induced immunity in older animals – lower worm burdens
4
Q
Ascarids adult worms describe the 2 main issues
A
1) Production and economic losses
- luminal feeders, malnutrition, reduced weight gain, stunting (young animals)
2) Clinical disease:
- diarrhea, colic, vomiting
- intestinal ileus, blockage, rupture -> peritonitis - most dangerous
- bile duct occlusion (cholestasis)
- gall stones (in humans)
5
Q
Ascarids larvae what are the 3 main things it causes in hosts
A
1) HPM cause mechanical and inflammatory damage to organs
○ Inflammatory is always eosinophilic
2) Milk spots in pigs – organ condemnation.
3) Eosinophilic pneumonia – calves, piglets, pups, kittens, foals (asthma-like signs -> looks like asthma attack)
○ Predisposes to viral and bacterial pneumonias
○ Damaged lungs do not regenerate! Foals -> race horsing
6
Q
Ascarids list the 3 zoonses issues
A
1) Adults of A. suum cross-infect humans
2) Larvae of Toxocara canis and T. cati cause ocular and visceral larva migrans
3) Larvae of anisakids cause eosinophilic\ gastritis (fish-borne zoonosis)
7
Q
Toxocara canis how are puppies infected
A
- Larvae reactivate during pregnancy
- Infect placenta go into foetus
- Born with infection (TP)
- Keeps getting infected via TM (L3)
8
Q
what occurs when dogs mature in terms of identifying infection
A
somatic vs tracheal migration -> No eggs ≠ no infection (esp. breeding females!)
○ As immunity develops larvae in the muscle but not necessarily within the gut -> somatically infected
○ Always ASSUME that the breeding animal has been infected
9
Q
How to differentiate between Toxocara and Toxascaris with eggs
A
Toxocara - cannot differentiate species based on faecal float, base on gender
- Egg is pitted - golf ball
Toxascaris leonina - egg is smooth
10
Q
How to differentiate between toxocara and toxascaris with structure of the worm for cats and dogs
A
CAT Toxocara cati Arrow shaped head Toxascaris leonina Narrow shaped head DOG - male worm Toxocara canis Rounded tip near spicule Toxascaris leonina Sharp tip near spicule
11
Q
Ascarids public health significance what are the 2 types of larval migrations within humans and when bad
A
1) Visceral Larva migrans - marked immune response only bad with high larval load - hepatomegaly, cough, usually self-limiting but can be serious - eosinophilic encephalities
2) Ocular larva Migrans - caused by single larva entering eye, decrease vision and loss, treatment unsuccessful
12
Q
What are the 2 genus of ascarids in birds, lifecycle, PPP, eggs in environment and hosts
A
- Ascaridia spp. (small intestine) and Heterakis spp. (caeca) of chickens, turkeys, geese, ducks
- Direct LC, PPP ~4-6 weeks
- Eggs take 2 weeks to embryonate, viable for ~1 yr -> not as resistant
- Earthworm transport hosts -> concentrate ascarids eggs within their gut - PROBLEM
13
Q
Ascaridia galli host, PPP, what are the 3 effects on the host
A
- chickens, turkeys, geese, duck
Chicks 4-8 weeks old: - after PPP
1) Larvae develop to adults in duodenal and SI wall -> synchronous eruption of larvae leads to enteritis ± haemorrhagic enteritis
2) Adult worms intestinal occlusion (up to 12 cm long!)
3) Nutritional deficiency -> increased susceptibility to disease, poor growth etc.
14
Q
Heterakis gallinarum host, pathogenicity in host, why and what should you learn from that
A
- Of little pathogenic significance in itself
○ May cause caecal thickening in heavy infections - Phoresy (one parasite helps the other)– transmission of Histomonas meleagridis (protozoa) through egg (survives in environment)
- Protozoa – non pathogenic in chickens but highly pathogenic in turkeys “black disease”
- Necrotizing typhlitis and focal necrosis of liver
- Do not mix chickens and turkeys together!
15
Q
How to differentiate between the two ascarids of birds
A
1) Heterakis - up to 1.5cm long
2) ascaridia - up to 12cm long
Eggs identical
16
Q
List 6 things the infective stage of ascarids have in common and that are important with management
A
- Paratenic hosts -> rodents, birds
- Essential period of development for egg to become infective
- Prolific eggs layers >200,000 per worm
- Sticky eggs
- Highly resistant in environment – years!
- Resistant to most disinfectants
17
Q
In what systems are ascarids are a problem and how to control them
A
Extensively raised cannot control - pay for production loss
Intensively raised can control -> decontamination via bleach (sodium hypochlorite, flame gun) to remove outer shell then kill
- rodent and pest control
- do not feed raw meat
- regular deworming - treat and quarantine new arrivals
18
Q
List 3 drugs that are good against larvae and 2 that are good against adults
A
Larvae - Moxidectin, milimycin, bendazole
Adults - Pyrantel, - Piperazine
19
Q
Specific treatment regime for ascarids in pigs when treat growes, sows and boards, sows before farrowing, when test herd and what to treat with
A
- growers at 8 weeks (one off)
- sows and boards every 3 months
- sows 7-14 days prior to farrowing
- test every 6 months
- In feed levamisole, ivermectin, fenbenazole, morantel, piperazine (narrow spectrum - only Ascarids)
20
Q
Specific treatment regime for ascarids in horses, how often treat foals and other control problems
A
- Deworm foals every two months (rotating MLs, BZs, pyrantel), starting at 2 months of age, for the first year of their life (10-12 weeks)
- Rotate pasture for mares and foals annually
- FEC prior to deworming spring and autumn in adults
21
Q
Specific treatment regime for ascarids in dogs, when start with puppies how often, how often for adults
A
- De-worm puppies first at 2 weeks of age and then q 2 weeks till 10 weeks old, then monthly till 6 months old
- Adult dogs, esp. males
○ Deworm depending on ‘risk’
○ Faecal examination 1-2 times per year
22
Q
How and when to treat pregnant dogs against ascarids
A
- Does not kill arrested larvae, but kills them once they enter circulation) to prevent TP and TM transmission to pups
- Fenbendazole 50mg/ kg daily PO from Day 40 of pregnancy to +14 days post whelping* - not done
- Selamectin topically 40d and 55d of pregnancy*
- Labelled use monthly moxidectin topically (Advocate, Revolution, Bayer) Likely!
23
Q
Specific treatment regime for ascarids in cats, how often with kittens, queens, adults and examples
A
- De-worm kittens first at 3 weeks of age and then 2 weeks till 10 weeks old, then monthly till 6 months old
- De-worm queen at same time!
- Adult cats
○ Faecal examination and deworm according to risk (e.g. roaming or indoor) - Prevent lactogenic transmission to kittens by applying selamectin, moxidectin or emodepside topically to queen at the end of gestation
24
Q
What are the 3 steps in the pathway of anisakis
A
1) Eggs past in faeces
2) Crutacean ingest L3
3) Two ways
1. Gets eaten directly by definitive host
2. Gets ingested by series of paratenic host
25
Anisakiasis what is it a disease of, how occurs, clinical signs and how to avoid
```
disease in humans
- Acquired through ingesting L3 in raw, insufficiently cooked or smoked fish
- Invasive (1 hour -2 days)
○ Penetrates gut mucosa
○ Eosinophilic gastritis, enteritis
○ Acute vomiting and diarrhoea
○ Allergic response to antigens
- Cook well or freeze >7d!
Prevents everything but allergic response
```
26
Oxyurids what common name and general characteristics
Pinworms - pointed end
- Adults in caecum, colon and rectum
- Direct life cycle, highly host-specific - not zoonotic
27
What are the 5 steps in the general lifecycle of oxyurids
1) Adult within the colon
- Females migrate to rectum and lay eggs in mucus plug cement into perianal area - ITCHY
2) Unembryoanted in faeces
3) 4-5 days to embryonate to infectivity
4) Eggs viable for 7-10days
5) Infection via ingestion
28
Oxyuris equi what special characteristic with adult and egg, what lead to in horse and diagnosis
- Bulb on anterior end
- Eggs have mucus plug
- Pruitus ani -> Self-mutilation -> scratching on back, ratty tail
- Diagnosis -> not in faecal flotation, sticky-tape method on the anus -> collect the eggs
29
Syphacia obvelata host, and clinical signs
in mice most commonly associated with disease
○ Anal pruritis + self-mutilation
○ Diarrhoea / intussusceptions or impaction
○ Rectal prolapse
○ Weight loss
30
Oxyurids what are 3 ways to treat/manage
- Long course of fenbendazole or piperazine in water, ivermectin
- Reduce overcrowding
- High standards of hygiene
31
Order Spirurida features: lips, oesophagus, spicles, egg and lifecycle
- Two lateral lips (or no lips)
- Oesophagus with anterior muscular and posterior glandular sections
- Unequal spicules
- Eggs with L1 (oviparous) or L1 (viviparous)
○ Eggs hatch quickly
- Indirect LC – arthropod IH - CONTROL
32
Oxyurids what type of oesophagus
Rhabditiform oesophagus
33
Oxyurids what is the main significance
heartworm
34
What is the general diagnosis and treatment and control of spirurids
Diagnosis Predilection site; morphology of worm, egg/L1
| Treatment & control - arthropod vector intermediate hosts
35
Habronema and Draschia what are they, what are the 6 steps in their ifecycle
stomach worm of horses
1) Adults in the stomach -> eggs with L1 larvae (embryonated)
2) L1 hatch in dung pat -> hatch straight away
3) Flies lay larvae within dung, larvae eat L1
4) L1-L3 within the maggot during development into a fly
5) Fly has infective L3 within
6) Few ways horse becomes infected
1. Horse eats the fly
2. L3 secreted onto the skin around the mouth -> horse then licks L3
3. Sometimes stay on skin and burrow -> no more development just cutaneous lesions
○ Cutaneous habronemiosis and draschiosis
36
Drachia megastoma what is it, intermediate host and pathogenesis
stomach worm of horse
- Musca IH (intermediate host)
Pathogenesis
- More pathogenic than Habronema
- Excess mucus secretion and catarrhal gastritis
- Chronic eosinophilic granulomatous nodule (1-10 cm) and ulcer caused by Draschia.
○ If near pyloric opening may cause obstruction
○ Perforate -> intestinitis
- Cutaneous draschiosis - most common clinical manifestation
37
Habronema microstoma and Habronema muscae what are they, intermediate host and parthenogenesis
IH - Stomoxys, musca
Pathogenesis
- Near margo plicatus (line in stomach demarcating glandular and non-glandular section); no nodule formation
- Small ulcerations, catarrhal gastritis (hyperplasia and hypertrophy of the mucus-secreting cells)
- Pulmonary 'habronemiosis'
○ Multiple abscesses filled with necrotic debris containing parts of nematode larvae. as well as massive eosinophilic inflammation around the lesions.
- Cutaneous habronemiosis - most common clinical manifestation
38
Habronema and Drachia what are they and what is important with diagnosis through eggs
stomach worms of horses
- Typical spirurid eggs
- Faeces or gastric lavage - flotation using solution of SG > 1.20 (e.g. salt + glucose)
- Challenging - eggs may not shed if adults within a granulomatous nodule -> trapped within
○ Therefore not often that you see eggs
○ no eggs DOES NOT EQUAL no infection
- Cutaneous lesions - biopsy -> chronic granuloma
39
Habronema and Drachia what are they, how to treat and control the different stages
- Hard to get rid of as hidden within the granulomas - may need long-term treatment
○ Removal of granulomas then anthelmintics
- Adults: Habronema: oxfendazole, moxidectin.
- Cutaneous lesions (L3): ivermectin, abamectin, moxidectin – effective against cutaneous lesions
- Chronic cutaneous forms: surgical debridement, cryotherapy, corticosteroids + MLs.
CONTROL
Fly control – dispose and compost manure, IGRs
○ Face and eye masks, fans and fly screens in stables etc.
40
Spirocerca lupi what is it, 7 steps in lifecycle and PPP
stomach worm of dog (Spirurida)
1) Adults within nodules in oesophagus
2) Eggs passed through fistula into lumen
3) Eggs with L1 passed in faeces
4) L3 develops within dung beetle (IH)
5) Most commonly dogs eat faeces with beetles
OR -> paratenic host (lizards, birds, rodents) that are ingested
6) L3 larvae penetrate stomach wall -> migrate circulation to aorta in chest
7) A few weeks later migrate through aorta wall into the oesophagus
○ MOST OF THE PATHOGOLOGY
PPP = 5-6months
41
Spirocerca lupi what is it and clinical signs
stomach worm of dog
- Common in tropical/ subtropical regions globally
- Sudden death due to haemothorax caused by ruptured aortic aneurism (ballooning -> causing it to thin and rupture) caused by migrating larvae
- Granuloma (oesophagus or aorta) may become neoplastic -> fibrosarcoma -> need to remove
○ Regurgitation, vomiting, weight loss -> chronic wasting disease
○ Granuloma can get large enough to push on spine and may cause paralysis
42
Spirocerca lupi what is it and diagnosis
```
stomach worm of dog
- Challenging as eggs may not be present in faeces if no fistula to lumen
○ Eggs heavy – S.G. > 1.2
- Endoscopy
- Radiography
```
43
Spirocerca lupi what is it and treatment and control
stomach worm of dogs
- Challenging as adults protected within granulomas
- Moxidectin (Advocate spot-on) prophylactic labelled use -> before granuloma formation
- Tx off-label use of doramectin, moxidectin and milbemyin for prolonged periods – up to 6 months (chronic)
- Surgical removal of sarcoma where feasible -> then give anthelmintics
○ Sarcoma -> fibrosarcoma (risk of neoplastic change)
- Aid feeding – upright position
Disallowing scavenging/ free-roaming - CONTROL - hard in the tropics
44
Cylicospirura felineus what is it, what is known about lifecycle, intermediate host and pathogenesis
```
stomach worm of cat
- Little known about life cycle
○ No aorta oesophagus migration
- Arthropod IH (beetles)
- Common in feral cats
○ cysts with 1-40 worms ± granulomas
```
45
Physaloptera praeputialis what is it, intermediate host and pathogenesis
stomach worm of cat
- Beetles, cockroaches (IH) + PH (lizards)
- Small teeth attach to mucosa to cause ulcers
- Catarrhal gastritis ± melena
46
Gnathostoma what is it, 6 steps in lifecycle and PPP
stomach worm of cat and dog
1) Eggs unembryonated when passed
2) Become embryonated and hatch in freshwater
3) L2 within copopod 1st IH
4) L3 within 2nd IH or paratenic hosts -> fish
5) Cats and dogs engulf fish
6) L3 penetrate stomach wall, migrate liver, re-enter stomach and embed in nodules
PPP = 4-7 months
47
Gnathostoma what is it, pathogensis and clinical signs
stomach worm of cat and dog
- Common in feral / semi-domesticated dogs and cats
- Adults embedded in submucosal gastric nodules with tract leading to gastric lumen
- Subclinical or similar signs as above
○ Gastritis, vomiting, anorexia
○ Peritonitis – perforated gastric wall
48
Gnathostoma what is it, diagnosis and treatment and zoonotic significance
stomach worm of dog and cat
Diagnosis and Treatment
- Characteristics uni-plugged eggs on faecal floatation
- Adults 2-3 cm long, hooked cephalic bulb
- Limited information on tx, but ivermectin may be efficacious
Gnathostomiasis in humans - SIGNIFICANCE
- Fish-borne zoonosis
- Dogs, cats, pigs -> DH
- L3 penetrate stomach and undergo larva migrans gets lost
○ Continues to migrate, once in subcutaneous tissue can see
- Highly pruritic subcutaneous swellings that move
49
Gnathostoma hispidum what is it, lifecycle and pathogensis
stomach worm (spirurids) of pigs
- Same life cycle as G. spinigerum
- Rarely pathogenic
- Heavy infections: ulcerations gastric wall
50
Physocephalus sexalatus what is it, intermediate host, where live and pathogenesis
Stomach worm (spirurids) of pigs
- Only really seen with extensive piggeries
- IH dung beetle
- Live on stomach wall
Rarely pathogenic, catarrhal gastritis, poor growth rates
51
Thelazia spp what is it, location, what need to differentiate between how and pathogenesis
eye worm (spirurids) of ruminants, humans, dogs
- Sitting on the surface of the eye, they move -> not within the eye
○ Differentiate between filaria -> dermal layers or within eye
- Mild to severe conjunctivitis and blepharitis are common
- Mechanically remove the worm -> cotton bud
- keratitis, including opacity, ulceration, perforation may develop
52
Gongylonema what is it, pathogenesis, intermediate host
spiruids of cattle
non-pathogenic just causes larval migration tract in oesophagys or rumen
cockroach intermediate host
53
Acuaria (Dispharyx) and Tetrameres what are they and pathogenesis
- Larvae burrow under mucosa of gastric mucosa and koilin of gizzard – inflammation - (can’t grind food well, weight loss chicks) vomiting, anorexia.
- Adults: Hypertrophy, fibrous nodular growths proventriculus, vomiting, anorexia.
54
Filarioidea features where found, what type of larvae, lifecycle and size
- As for spirurids
- Adults NOT in GI tract – liquid diet (blood, lymph)
- Primarily viviparous (L1 = microfilaria)
- Indirect LC – arthropod IH (mosquitoes, flies, ticks)
- Adults are usually long (10 cm -1 m; females>males)
55
What are the 4 main diseases of Filarioidea
1. Queensland itch -> dermal lesions
- Microfilaria -> as pathogenic as the adults
2. River Blindness -> inflammation within the eye and lenses
3. Cattle filaria -> adult and microfilaria
- Transmitted by buffalo fly
4. Canine heartworm
56
Brugia malayi what is it, host, where found, and what lead to (pathogenesis)
Filarioidea of humans
- Adults in lymphatics, blocking drainage lymphoedema
○ Secondary infections skin (elephantiasis)
○ Irreversible damage
○ Arthropod borne
- Program to eliminate lymphatic filariasis by 2020
○ Mass administration of albendazole + either Ivermectin or DEC
○ Goal is to block transmission
57
Onchocerca volvulus what is it, host, what leads to
Filarioidea of humans
‘river blindness’
- Adults in ‘nests/clusters’ in SC tissue
- Microfilaria cause pruritic dermatitis “lizard skin”
- Microfilaria death in eye – inflammation -> blindness
58
Loa Load what is it, host and pathogenesis
Filarioidea of humans
| adults live in the subcutaneous tissue with affinity for the area around the eyes -> within the sclera
59
Onchocerca cervicalis what is it, host, where found and what causes in host
```
Filariodea of equids
adults in nuchal ligament
○ Oedema
○ Chronic granulomatous nodules and fibrosis (older horses)
- onchocerciasis
```
60
Onchocerca reticulata, what is it, host, where found and vector
Filariodea of equids
- (exotic) adults in flexor tendons
- Vector (IH) Culicoides spp - specific to the area
- onchocerciasis
61
Onchocerciasis horses what occurs, where on the host and the disease
- Dying microfilaria in dermal tissue leads to pruritic dermatitis -> antigenic release
- Skin of the ventral midline, face, neck, chest, withers, forelegs, and abdomen.
- Scale, crusts, ulceration, permeant alopecia and depigmentation
- “Queensland itch” or “Neck worm” -> lots like hypersensitivity to flies
62
Onchocerciasis horses how to diagnose and treat
- Skin snip (warm saline) or biopsy (histopathology) – drastic?
○ Microfilaria rarely in blood
- Response to treatment -> probably don't need to diagnose
- Ivermectin and moxidectin highly efficacious against microfilaria
○ Marked clinical improvement
- Permethrin pour-ons
63
Onchocerca gibsoni what is it, host, location in host, and what is the major issue
Filarioidea of cattle
- in the brisket of cattle
- Carcass trimming and condemnation major loss to beef industry in northern Australia
- Forms nodules with worms within
64
Stephanofilaria stilesi what is it, vector, where live in host, pathogenicity
Filarioidea of cattle
- Vector Haematobia irritans or the ‘buffalo fly’
- Adults live within dermis. Microfilaria also cause pathogenicity
○ Lesions ventral thorax and abdomen
§ Ulcerated and exudative (fly attractant)
Chronic – hyperkeratosis, pigmented
65
Stephanofilaria control
- Challenging!
- No anthelmintic effective vs adults
- Northern and coastal northern NSW
- Buffalo flies cannot live off host > 1-2 hr
- Non-chemical control options
○ Walk through fly traps
○ dung beetles
- Synthetic pyrethroids or OPs
- Pour on, ear tags, dips etc.
66
Diagnosis of filarioids in cattle
- What’s in your area? Ask abattoir! – predilection sites of adults
- Skin snip, macerate in warm saline
- Stephanofilaria mff tiny (~50 μm) c.f. Onchocerca and Setaria > 230 μm
67
Dirofiliaria immitis what is it, host and the 8 steps in the lifecycle
Filarioids of dogs
1) Adult worms in pulmonary artery within pulmonary vessels
2) Produce L1 - vivparous - microfilaria
3) Circulation in blood for years and taken up by mosquitoes
4) Moult within mosquito to L3 - 2 weeks
5) Inject L3 (infective) into blood stream of new host
6) Larvae migrate to muscles of chest and abdomen L4-L5
7) Eventually move to pulmonary artery -> induce eosinophilic response before adult 2-4 months
8) 2-4 months to become patent and produce microfilaria -> move into right ventricle
IMPROTANT FOR TREATMENT
68
Dirofiliaria immitis what are the 5 main features of the pathogenesis
1) Presence of worm and its endosymbyont (Wolbachia - bacterium)
2) Proliferative endarteritis of pulmonary arteries (thickening) -> decreased compliance
PLUS
Thrombosis and thromboembolism (especially dead parasites)
3) Pulmonary hypertension
4) ↑ Afterload for the right ventricle - Right ventricular hypertrophy and dilation
5) RSCHF (right sided heart failure) ± caval syndrome (when lots and lots -> mechanical problem)
69
What are the 2 main diseases from dirofiliaria immitis IN DOGS
1) Pulmonary Arterial diseases (PAD) - acute
| 2) Caval Syndrome - chronic stage
70
Pulmonary Arterial Disease (PAD) what causes it and what occurs, clinical signs
Dirofiliaria immitis
- Myointimal proliferation -> villus proliferation of endothelium; inflammation; leakage
- Oedematous lungs
- First signs -> cough -> sounds like kennel cough
71
What are the 3 main ways to diagnose heartworm
1) History and clinical signs - travel and prophyaxis
2) detection of microfilaria in blood and antigens
3) Antigens test for adult worms
72
Detection of microfilaria in blood and antigens how used and what are the 3 main problems
- Unstained fresh wet smear or buffy coat (insensitive) - may be able to see
- Concentration methods
○ Knotts test - important use formalin that enables you to differentiate their morphology
○ Filtration method
1) False negatives due to occult infection -> Up to 30% of infections may be occult - not producing microfilaria
2) no indications of worm burdens
3) other filarial species -> need to morphological distinguish
73
List the 5 reasons for a occult heartworm infection
1. Single worm infections
2. Pre-patent infections or geriatric worms - do not test before 6 months of age
3. Ectopic infections - adults don't enter pulmonary artery
4. Drug induced elimination (e.g. ivermectin) or sterility (e.g. doxycycline) - ask client whether treated
5. Immunologically mediated elimination of microfilaria -> evolution overtime in tropics
THEREFORE NOT SEEING THEM DOESN'T MEAN NOT NEGATIVE
74
Antigen tests to adult female worms what does it need and what is the problem with it
○ At least 3 females needed for consistent results
○ Sp (96-100%) and Se (90-96%)
○ Beware – PPV and NPV when interpreting test in low prevalence area
○ If negative again doesn't been doesn’t have it
75
Antigen tests to adult female worms what does it need and what is the problem with it
○ At least 3 females needed for consistent results
○ Sp (96-100%) and Se (90-96%)
○ Beware – PPV and NPV when interpreting test in low prevalence area
○ If negative again doesn't been doesn’t have it
76
What are the 3 main images that suggests heartworm infection
1) enlargement of teh heart
2) abnormal lung patterns
3) ultrasound - hyperechoic parallel lines
77
What are the 3 steps in the treatment for heartworm
1) supportive care
2) prevent new infects and kill microfilaria
3) kill adults
78
Heartworm treatment: Step 2: prevent new infection and kill microfilaria what is the main drug and how to administer over how long
- Macrocyclic lactones (monthly or injectable) commenced on Day 0
○ Prevents new infections
○ Kills circulating mff over 7-10 days (if too quick, anaphylaxis, so care under observation 24 hr!)
§ Most of these treatments are monthly
§ If don't respond within 7-10days may have resistance
○ Over longer term – 4 -12 months (kills juveniles and adults)* - slow kill treatment
§ Not recommended due to ability to acquire resistance
79
Heartworm treatment: Step 2: prevent new infection and kill microfilaria what is the main drug and how to administer
- Macrocyclic lactones (monthly or injectable) commenced on Day 0
○ Prevents new infections
○ Kills circulating mff over 7-10 days (if too quick, anaphylaxis, so care under observation 24 hr!)
§ Most of these treatments are monthly
§ If don't respond within 7-10days may have resistance
○ Over longer term – 4 -12 months (kills juveniles and adults)* - slow kill treatment
§ Not recommended due to ability to acquire resistance
80
Caval Syndrome what are the 2 main treatments and the problems
Surgical extraction of worms cannot kill them as they are causing mechanical damage
Alternative Regimes “soft kill”
- If melarsomine is not available - some countries
- ML + doxycycline (10 mg/kg bid, 1 month on, 2 months off etc.) over 9 months – 12 months shown to kill adult worms
- Problem: Clinical signs may develop or worsen in the interim - not in the clinic so cannot monitor
○ Don’t know when adults dying!
○ Resistance!
81
What are the 2 main clinical signs of acute diseases caused by heartworm infection IN CATS
1) Heartworm Associated Respiratory Disease (HARD)
○ Acute disease as result of larvae arriving, even if destroyed
○ Pulmonary arteriole hypertrophy, pulmonary oedema – tachypnoea, cough, vomiting, weight loss
2) Usually result from embolus of dead worms, not presence of worms themselves
○ None - no clinical signs - sudden death
○ Severe dyspnoea, haemoptysis, collapse, sudden death
82
What are the 3 main ways to diagnose heartworm infection in cats
challenging:
1) Antibody test – early as 8 weeks post-infection
2) Antigen tests if >1 adult female
3) Radiographic changes HARD
○ ± bronchialveolar pattern
○ ± slight enlargement of caudal lobar arteries
○ ± or adults on ultrasound
83
What are the 2 main treatment options and what are contraindicated in heartworm in cats
○ Prednisolone - reduce inflammation in case the worm dies
○ Surgery if worms visualised in ‘reachable’ area
○ Adulticides contraindicated
84
Enoplids type of lifecycle, special feaure, male features and what type of eggs
- Most direct life cycles (± transport hosts e.g. earthworm)
- Non-muscular stichosome oesophagus (mostly glandular)
○ Becomes embedded into mucosa - secretes enzymes
- Male with single (ensheathed) spicule or no spicule (Trichinella)
- Female
○ oviparous (thick-shelled, lemon-shaped egg; bipolar plugs) or
viviparous L1 = infective stage*
85
Enoplids type of lifecycle, special feaure, male features, what type of eggs and ZOONOSES
- Most direct life cycles (± transport hosts e.g. earthworm)
- Non-muscular stichosome oesophagus (mostly glandular)
○ Becomes embedded into mucosa - secretes enzymes
- Male with single (ensheathed) spicule or no spicule (Trichinella)
- Female
○ oviparous (thick-shelled, lemon-shaped egg; bipolar plugs) or viviparous L1 = infective stage*
All are zoonotic
86
Trichinella what order and the lifecycle including the 2 cycles
Order: Enoplida
1) L1 is infectious and is within the muscle
2) If next host eats L1 within muscle
3) Adult within the intestines -> produce L1
4) Adults die and L1 move into muscle
Two cycles
1) Domestic - pigs and rodents
2) Sylvatic cycle - bears, rodents, rhino
Humans -> dead-end hosts
87
What are the 2 types of Trichinella hosts and where found in host
1) encapsulated species
- Mammals only
- L1 surrounded by collagen capsule or ‘nurse cell’ within muscle tissue
2) Non – encapsulated species
- Mammals, birds, reptiles, marsupials
- L1 ‘free’ in muscle tissue
88
What is the main disease caused by trichinella in humans, how transmitted and is there disease in usual hosts?
Trichinellosis
- Major meat-borne zoonoses
○ Eating raw or undercooked meat
○ Domestic pork - T. spiralis
○ Hunted game meat - feral pig, cougar, bear, crocodile, walrus
- Major economic + Public health significance
ANIMALS - NO DISEASE
89
Trichinellosis what are the 2 main stages of disease with clinical signs and treatment and diagnosis
- Severity α dose ingested
1) Per-acute (intestinal phase)
○ Diarrhoea, abdominal pain, vomiting, fever - enteritis
2) Acute (muscle invasion): 2-8 weeks
○ Eosinophilia, elevated CK
○ Myalgia, fever
○ Vasculitis ± cardiac / neurological complications -> death
Treatment: Corticosteroids and albendazole to kill L1 stage
Diagnosis by serology
90
What are the 3 main risk factors for trichinellosis and describe
1) Poverty
- Cannot afford to feed pigs
2)animal husbandry practices
○ Allow roaming and scavenging
- Backyard slaughtering
- Lack of meat inspection
3) Meat preparation
- Proper cooking to over 77ºC
- Microwaving ineffective
- Salting (<2%) or smoking ineffective
91
What are the 2 prevention and control methods used by countries to prevent trichinellosis
Meat Inspection and Certification - for exports
1) Freezing
○ - 20ºC for 2 weeks kills T. spiralis
○ All exported farmed pork in Australia freeze certified (-20 for 4 weeks)
§ Too expensive so pork isn't exported
○ T. nativa survives -20ºC for 6 months
2) Testing: Artificial Digestion Methods (HCl acid + Pepsin) and visualisation of larvae
○ Technique of choice by EU - costs a lot of money
○ 5 g of diaphragm of ‘high-risk’ meat
92
Trichuris special feature, features of the eggs
- ‘Long ‘whip’ is the stichosome (modified glandular oesophagus)
- Bury their stichosome deep into mucosa, digests tissue and ingests fluid
- Eggs take 3 weeks to embryonate
- Eggs highly resistant (4-5 years in environment) - similar to ascarids
93
What are the 5 steps in the trichuris lifecycle, what age likely in (why) and PPP
1) Small intestines where stay through development
2) Larvae migrate to large intestines where mature to adults
3) Pass eggs in the faeces (lemon shaped eggs)
4) Take 3 weeks to embryonate
5) Ingested by host (dog)
NO TRANSMAMMARY, TRANSPLACENTAL - less likely in puppies - older animals
PPP = 10-12 weeks
94
Trichuris what are the main effects and clinical signs
- Heavy infections: congestion, submucosal oedema, epithelial desquamation, necrosis, fibrosis (mass)
- Colitis (adults in colon) -> Watery and mucoid diarrhoea ± blood (frank - fresh)
- Tenesmus - straining to defecate -> Rectal prolapse
95
Trichuris Suis where belong, diagnosis and treatment
```
Class: Nematodes
Order: Enoplida
Diagnosis
- Eggs are heavy – SG ≥1.20 (saturated salt + glucose)
- Lemon shaped
Treatment:
- Oxantel (usually in combo)
- MLs (except selamectin)
- BZs e.g. fenbendazole , albendazole (3 days), febantel (pro-BZ in combo) single dose.
```
96
Capillaria of poultry vector and what occurs with light and heavy infections and treatment
- Eggs embryonate in soil or within earthworms (transport host - eat eggs and larvae within)
Light infections
- Poor weight gain, lowered egg prod.
Heavy
○ Catarrhal thickening, diphtheritic inflammation of oesophagus and crop
○ Catarrhal, haemorrhagic enteritis
○ High mortality
Treatment ->
ivermectin, BZs (fenbendazole), levamisole
97
Acanthocephala features, size, shape
- Dioecious (males and females)
- Cylindrical in shape
- Usually quite large
- Proboscis with hooks/spines (pathogenic effect) -> inject and latch on to organs
- No digestive tract! -> lots of reproductive organs
“Bag of reproductive organs with a holdfast”
98
Macracanthorhynchus hirudinaceus what is it, hosts, location in hosts, pathogenesis and treatment
Phylum Acanthocephala
Intermediate hosts -> Arthropods
- Dung beetles, cockroaches
Definitive host -> Pig, rodent, humans
Small intestine and duodenum of definitive host
- Granuloma at site of attachment, enteritis +/- perforation
Treatment
- Ivermectin, levamisole, BZs - off label -> not registered drug
99
Oncicola spp what is it, where common in what hosts and effects on host
Phylum Acanthocephala
- Common in small intestines of feral or stray dogs and cats
- Usually asymptomatic +/- enteritis
