Parasitology NEM Flashcards
Ascaridida features how large, what eat, special structures and the eggs
- 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
List the 10 steps in the lifecycle of ascards
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
Ascarids significance how common, what age and why
- Common! Usually young hosts < 1 year
- Strong exposure induced immunity in older animals – lower worm burdens
Ascarids adult worms describe the 2 main issues
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)
Ascarids larvae what are the 3 main things it causes in hosts
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
Ascarids list the 3 zoonses issues
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)
Toxocara canis how are puppies infected
- Larvae reactivate during pregnancy
- Infect placenta go into foetus
- Born with infection (TP)
- Keeps getting infected via TM (L3)
what occurs when dogs mature in terms of identifying infection
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
How to differentiate between Toxocara and Toxascaris with eggs
Toxocara - cannot differentiate species based on faecal float, base on gender
- Egg is pitted - golf ball
Toxascaris leonina - egg is smooth
How to differentiate between toxocara and toxascaris with structure of the worm for cats and dogs
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
Ascarids public health significance what are the 2 types of larval migrations within humans and when bad
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
What are the 2 genus of ascarids in birds, lifecycle, PPP, eggs in environment and hosts
- 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
Ascaridia galli host, PPP, what are the 3 effects on the host
- 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.
Heterakis gallinarum host, pathogenicity in host, why and what should you learn from that
- 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!
How to differentiate between the two ascarids of birds
1) Heterakis - up to 1.5cm long
2) ascaridia - up to 12cm long
Eggs identical
List 6 things the infective stage of ascarids have in common and that are important with management
- 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
In what systems are ascarids are a problem and how to control them
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
List 3 drugs that are good against larvae and 2 that are good against adults
Larvae - Moxidectin, milimycin, bendazole
Adults - Pyrantel, - Piperazine
Specific treatment regime for ascarids in pigs when treat growes, sows and boards, sows before farrowing, when test herd and what to treat with
- 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)
Specific treatment regime for ascarids in horses, how often treat foals and other control problems
- 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
Specific treatment regime for ascarids in dogs, when start with puppies how often, how often for adults
- 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
How and when to treat pregnant dogs against ascarids
- 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!
Specific treatment regime for ascarids in cats, how often with kittens, queens, adults and examples
- 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
What are the 3 steps in the pathway of anisakis
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
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
Oxyurids what common name and general characteristics
Pinworms - pointed end
- Adults in caecum, colon and rectum
- Direct life cycle, highly host-specific - not zoonotic
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
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
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
Oxyurids what are 3 ways to treat/manage
- Long course of fenbendazole or piperazine in water, ivermectin
- Reduce overcrowding
- High standards of hygiene
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
Oxyurids what type of oesophagus
Rhabditiform oesophagus
Oxyurids what is the main significance
heartworm
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
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
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
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
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
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.
