----start parasit.lec.09.04.97----

parasitology
Dr Colin Johnstone

Lecture 4 "trichostrongylodea" continued


http://phl.vet.upenn.edu/cal95/parasit/tricho/indextricho.html

parasites 
in and of themselves are capable of causing dz. 
arthropods in particular 
also often act as vectors for other dz.

again a recap of the NEMATODES 
OF VETERINARY IMPORTANCE

nematodes divided into bursate and non bursate 
nematodes

bursate nematodes are the order strongylida (have copulatory 
bursa - critical functional feature for sexual reproduction). In the 
order strongylida are four superfamilies of trichostrongyloidea, 
metastrongyloidea, and strongyloidea, and ancylostomatoidea (which are 
sometimes considered part of the strongyloidea superfamily).

non bursate 
nematodes are ascaridida, rhabditida, enoplida, oxyurida, and sprurida.


so far we've classified the nematodes and gone over the basic nematode 
life cycle. 

The TRICHOSTRONGYLOIDEA are divided into two families

Trichostronylidae - contains 6 genera: haemonchus (important in sheep, 
cattle; voracious blood feeder), cooperia, hyostrongylus, etc.

anyway.


OSTERTAGIA: small roundworms, about a cm long. predilection site for all 
species is the abomasum of ruminants. major cause of gastritis in 
ruminants in temperate areas.  three species: o.ostertagi in cattle, and 
o. circumcincta and o. trifurcata in sheep and goats. o. ostertagi is 
hugely important in cattle

life cycle of o.ostertagi. 
adult 
males/females are found in mucosal surface of abomasum. females lay eggs 
which are passed in feces of host and deposited on pasture. this is a 
direct life cycle - no intermediate hostss. preparasitic stages are all 
freeliving in environment. L1 grows in egg. egg hatches. L1 grows, molts 
to L2, L2 grows, molts to L3 (ensheathed). this all occurs in feces on 
pasture. then rainfall activates L3 to migrate onto pasture, away from 
feces. L3 is ingested by grazing ruminant. L3 exsheaths in rumen, passes 
into abomasum, gets into abomasal glands, molts into L4-then L5 - then 
becomes adult and gets onto abomasal mucosal. prepated period 3 weeks 
unless arrested development occurs. a.d. important in this lifecycle. 
then we see arrested L4 in the abomasal glands.

CLINICAL SIGNS
diarrhea

anorexia
wt loss

this is the commonest cause of parasitic gastritis in 
cattle. most commonly affects young cattle grazing for first time. see 
watery diarrhea, anorexia, wt loss. in acute cases, you can see 20% wt 
loss in 7 days.  

because of the hypobiosis, ostertagiasis occurs in two 
forms: type I and typeII

type I: classical form, as described above. 
occurs in cattle during first grazing season, as result of normal 
development w/prepatent period about 3 wks

type II usually occurs in 
older animals, yearlings, after first grzing season - in late 
winter/early spring in northern temperate regions. used to be "winter 
dysentery" - it is the result of arrested larvae from the year before 
resuming development all at once. the abomasal glands are disrupted. 
diarrhea ensues.

epidemiology:

important factors: in more temperate 
areas, significant numbers of larvae survive over the winter. but even if 
no larvae survive the winter, hypobiosis allows some to survive. it they 
do survive on pasture , they may be able to produce disease in naive 
animals. if number is insufficient to cause clinical syndrome, will still 
be enough to cause infections, which will cause contamination of pasture, 
which will result in disease occuring later in season. eg, "seeding" of 
pasture with eggs that effect other animals later in grazing season.


early preparasitic period very dependent on temperature- 
egg--->L1--->L2--L3 happens faster in warmer weather. as summer arrives 
you see more and more L3 on the pasture, a buildup to a dangerous stage 
wrt development of clinical dz.

hypobiosis in temperate zones is 
signalled by dropping temp in fall of year. maturation occurs in late 
winter/early spring, and is responsible for type II disease. in southern 
states, arrested development triggered by a dry season, not by coldness 
(not usually cold there...) so we see type two disease there in late 
summer/ early fall.

slide: male worm and arrested L4.

ostertagiasis 
diagnosis: ostertagia has a strongyle type egg, so can't speciate by egg 
alone. if you have animals you suspect of ostertagia infxn, you look at 
grazing history, clinical signs, fecal egg counts, plasma pepsinogens (- 
due to disruption of abomasal glands, abomasum leaks pepsinogen into 
plasma), response to tx, and necropsy.

note: "diagnosis is the thing. 
any fool can treat." but sometimes you do not know the diagnosis, but you 
MUST treat. so you often, in the field, use the treatment to determine 
the dx- eg, if animal recovers, you were likely correct.

next genus:


NEMATODIRUS all species live in small intestine.
slender, long worms up 
to 2.5 cm long. inflated cuticle at anterior end. females pass 
distinctive eggs - about 4x the size of a strongyle type egg, with a few 
large brown granules.

in the field, this parasite is important when 
present with other parasites as well. you normally see mixed parasite 
infections...and usually, one of them is the predominant pathogen in a 
given location. in most temperate areas in sheep and cattle in this 
country, ostertagia is the main one. in humid warm areas, hemonchus will 
be (like here in the summer).

but n. battus CAN be a primary pathogen in 
lambs born in late winter/early spring. this is due to its life cycle. L3 
develop within protective egg. So, egg develops L1, grows into L2, grows 
into L3 all inside egg. In n.battus, L3 must experience  a freeze 
followed by rise in temperature before it will hatch. so all the eggs 
hatch at the same time, pretty much.

trichostrongylus, haemonchus, and 
ostertagia all exhibit typical nematode life cycle. but nemotidirus 
doesn't. larval development through L3 occurs inside the egg.

next genus


COOPERIA

all found in small intestine
infect ifferent species but cause 
same kind of pathology, similar life cycles
small worms. most 
distinguishing features - slightly inflated cuticle anteriorly, and they 
tend to have coiled bodies.

life cycle basically like others
direct, no 
intermediate hosts. arrested development plays important part. like 
nematodirus, these are secondary pathogens. added to effects of 
ostertagia and hemonchus. 

new genus

HYOSTRONGYLUS

HYOSTRONGYLUS 
RUBIDUS red stomach worm of pigs
is found in stomach, and appears red 
because it is a blood feeder, though not as voracious as haemonchus. 
primary cause of hemorrhagic gastritis characterized by anemia and 
diarrhea. used to be major pathogen until 10 yrs ago. now there have been 
changes in swine industry and more pigs are raised inside so they don't 
see this worm that much. passes strongyle type egg. similar to 
oesophagostomum dentatum and trichostrongylus axei
hypobiosis is 
important
long reddish worm. males have copulatory bursa.

LEAVING 
TRICHOSTRONGYLIDAE FAMILY

NEW FAMILY

DICTYOCAULIDAE (member of 
trichostrongyloidea superfamily)

only one important genus here: 
DICTYOCAULUS
this worm parasitizes the lungs not the GI tract like all 
the others did. This is why they are in a different family - different 
predilection site

3 spp
filaria - sheep and goats
viviparus - cattle

arnfeldi - horses/donkeys

predilection site: bronchi in all species. 
white, thin, threadlike worms in bronchi and bronchioles are readily 
seen. anywhere from 3-8 cm long. they are bursate, remember. the males 
have copulatory bursa.

d.viviparus (most stuff also applies to other 
spp): it's found worldwide but commonest in temperate areas. in us, seen 
in NE and pacific NW. doesn't like heat at all. so in SE PA near us we 
rarely see this. but we do see it in other areas of the state. NW PA and 
the poconos do have dictyocaulus spp. you may see sporadic outbreaks of 
this in grazing animals through the summers in those areas.

life cycle


adult males and females in bronchi of host. female lays eggs that are 
already embryonated so they hatch nearly immediately into L1. L1 migrate 
up bronchial tree, get coughed up and swallowed, then pass out with feces 
as L1. on pasture, preparasitic L2 and L3 develop. 

one thing about 
ostertagia was that preparasitic phase occurs in feces of host. then 
rainfall caused L3 to migrate away from feces onto pasture.

dictyocaulus 
larvae are not very motile. 
grazing cattle do not eat where they 
defecate.
so dictyocaulus larvae have to get a way to get out of the 
feces. they have an interesting way of doing this. what they do is, L3 
migrate onto the sporangia of a pilobilus fungus (SP??) so when sporangia 
explodes, larvae are dispersed onto pasture. this fungus grows in cow 
manure. they can disperse as much as 10 ft away! so this is a unique 
adaptation.

L3 ingested by host
L3 (small intestine)---> migrates to 
mesenteric LNs---> L4
L4-->lymphatics-->blood-->lungs
L4--->migrates to 
bronchioles--->adult

prepatent period (from ingestion to L1 in feces) 
about 3-4 wks

bronchitis w/coughing can occur before patency as L4 
migrates through lungs.
patent dz is associated with adult worms in the 
bronchi. easy to dx this nematode infxn by looking for L1 in feces. 
patent dz manifests as bronchitis and coughing followed by pneumonia 
caused by aspiration of eggs and L1 into the lungs. also emphysema. if 
progresses to emphysema, prognosis poor. secondary bacterial pneumonia 
often kills host.

epidemiology: once animals are infected the second 
time, there is a stong immune response (remember, they migrate to LNs). 
so in europe they have a vaccine - an irradiated L3, given orally. L3 
will molt from L3-->L4 in the LN but then will stop and animal will have 
immune response. in temperate areas lg numbers of these larvae will 
overwinter. hypobiosis is important but they arrest at immature adult 
(L5) stage, not L4. immunity will occur in older carriers but immunity is 
not absolute - so these animals continually seed pasture with small 
numbers of L1. their own infections are at very low levels but they 
present a danger to younger naive animals. the vaccine is very effective 
but is not available in the US for various annoying reasons.

diagnosis: 
occurs seasonally. clinical signs - coughing. confirm via L1 in feces.


d. arnfeldi is found in donkeys and horses but donkeys tolerate it very 
well, and rarely develop clinical dz. but in horses it can cause chronic 
coughing.

----end-----