Transmissible
Gastroenteritis
Associated w/ Small
Intestine & Brain Lesion in
Piglets in a Commercial
Farm
PRESENTED BY: SOL KIZZIAH MEI R. CABANDI
OVERVIEW
OVERVIEW
The case study report described a transmissible
gastroenteritis coronavirus (TGEV) infection presented in a
commercial pig herd.
The clinical signs of infection appeared in newborn piglets,
included medium morbidity and low mortality rates.
Rectal swabs were collected from five different affected
litters for laboratory examinations.
OVERVIEW
Samples from two dead piglets and two euthanized
affected piglets were collected for gross and
histopathological examinations.
All fecal samples were tested TGEV positive by real-time
polymerase chain reaction (RT-PCR).
Necropsy revealed nonspecific gross lesions.
OVERVIEW
The histopathological examinations revealed villi fused
with denuded tips and severe villus atrophy, leading to
extensive epithelial flattening in middle and lower small
intestine.
The architecture pattern of villi presented columnar and
cuboidal poorly differentiated enterocytes with mild
subepithelial edema.
In some enterocytes, pycnotic nuclei were detected.
OVERVIEW
Microscopic examination of brain tissue revealed diffuse
gliosis in the area of pia matter with mild congestion of
the meningeal and parenchymal vessels and neuronal
degeneration.
In conclusion, this case study reported an epidemic TGEV
infection in piglets, characterized by low mortality and
medium morbidity rates accompanied by typical
histopathological lesions in small intestine, as well as by
coexisting brain lesions, that are described for the first
time.
INTRODUCTION
INTRODUCTION
Transmissible gastroenteritis (TGE) in
swine is one of the most significant
diarrhea-producing diseases in young pigs.
Transmissible gastroenteritis
coronavirus (TGEV), belongs to
Alphacoronavirus genus and
Coronavirinae subfamily.
TGEV is a subspecies of the
Alphacoronavirus 1 species.
INTRODUCTION
On a herd basis, two epidemiological forms of TGE are
recognized: epidemic and endemic.
Epidemic:
Typical clinical signs of epidemic TGEV
infection
Piglets: vomiting and diarrhea (profuse watery,
yellowish), rapid loss of weight, dehydration, and
high morbidity and mortality rates in piglets of <2
weeks of age
Finishing swine and in sows: inappetence, transient
diarrhea, and vomiting
INTRODUCTION
Endemic:
Typical clinical signs of endemic TGEV
infection
mild diarrhea in piglets ~6 days of age
The consistency of the feces ranges from clear and
watery to white and creamy, and in late-stage
disease it becomes gray and pasty.
Low mortality (usually <10–20% in pigs from 6 days
of age until 2 weeks after weaning) and concurrent
infection are characteristic, although some litters
may experience severe clinical signs.
INTRODUCTION
Endemic:
Severity of clinical signs is dependent on the age of
pig, the management system, degree of exposure to
the virus, and degree of passive maternal immunity.
Infected sows usually do not show clinical signs.
INTRODUCTION
The caused acute maldigestive/malabsorptive
diarrhea and the dehydration in piglets are due to a
marked reduction in enzymatic activity in the small
intestine, resulting in a disruption of digestion and
cellular transport of nutrients and electrolytes.
The main caused lesion of TGE is markedly shortened
villi of the jejunum and ileum. Villous atrophy is more
severe in newborn pigs than in older pigs, as neonates
are more susceptible to TGEV infection.
CASE DESCRIPTION
CASE DESCRIPTION
Description of the Farm
Breeding stock of a farrow-to-finish commercial pig
farm (commercial hybrids of Large White Landrace) in
Central Greece
Farm capacity: 550 sows under production
A grandparent nucleus of 40 sows was kept in the farm
for producing its own gilts.
CASE DESCRIPTION
Farm Facilities
12 farrowing houses 10 pens
18 flat-deck units 2 pens of 55 animals
Growing houses 46 pens of 50 animals
One finishing house 4 pens of 40 animals
One mating-pregnancy (dry period) stable 0–35th day of pregnancy
with 240 individual stalls
Two breeding stock house of group housing 18 pens of 10 sows/35–105th day of
pregnancy
One breeding stock house of group 5 pens of 25 gilts
housing for non inseminated gilts
A feed mill
An artificial insemination laboratory
CASE DESCRIPTION
Description of the Farm
The herd practiced a 1 week batch production system.
The weaning piglets were allotted equally according to
the body weight and sex at random at flat-deck batteries
for piglets in a climate controlled postweaning stable.
CASE DESCRIPTION
CASE DESCRIPTION
Description of the Farm
Breeding females – given single ivermectin inj. 14 days
before farrowing
Boars – 2x a year (ivermectin)
Feed – corn/barley/wheat-soya meal (changes per season)
Breeding animals – different feed during
gestation/lactation
Drinking water - ad libitum
Housing facilities - fully automated temperature and
humidity control system, automated feeding.
CASE DESCRIPTION
Disease Progression
Nov 2017 – 1st clinical sign: vomiting, ff by diarrhea in 5
pens at 1 of 12 farrowing houses
Age of newborn piglets: 1 to 4 days old (all sows were at
first parity)
In the beginning, diarrhea was very sparse, watery, ran
down the hind legs, and dripped from the tail.
CASE DESCRIPTION
Disease Progression
As the disease progressed, diarrhea was more
obvious, more specifically thickened, becoming
yellowish and foamy
The skin of the rump was usually wet and soiled.
CASE DESCRIPTION
Disease Progression
Subsequently, the piglets became dehydrated and
had eyes that were sunken
Their hair coat was also quite rough and presented
significant weight loss.
In a week interval, all pens (totally 10) of the
farrowing house were affected by diarrhea.
CASE DESCRIPTION
Disease Progression
Morbidity rate: medium (*30–35%)
Mortality rate: low (<8%), mainly due to severe
dehydration
In the following weeks, diarrhea was observed in other
two farrowing houses, where the 50% were at their first
parity.
DIAGNOSIS
DIAGNOSIS
Sampling
A combination of different tests was carried out so that
to have an accurate diagnosis of the cause of the
infection.
Fecal samples (rectal swabs) were taken from five
different affected litters (five samples from live piglets 1–
4 days of age/ litter) for laboratory examinations (real-
time polymerase chain reaction [RT-PCR], bacteriological
testing).
DIAGNOSIS
Sampling
In addition, three of the aforementioned piglets with
symptoms were euthanized, and sent to laboratory for
necropsy and histopathological examinations.
DIAGNOSIS
Laboratory examinations
Fecal samples were examined by RT-PCR for TGEV and
rotavirus infection.
This method allows the rapid and sensitive detection of
RNA of TGEV from samples purified from nasal swabs
and feces.
A specific RNA sequence of the TGEV genome is
transcribed into cDNA and amplified by the RT-PCR,
which is applied on Light Cycler 2.0 Roche® .
DIAGNOSIS
Laboratory examinations
Specific primers and probes are used to amplify and
detect a part of the S region of TGEV.
Using the Taqman probes principle maximizes the
specificity of this method.
DIAGNOSIS
Laboratory examinations
The euthanized piglets were autopsied to find any gross
lesions. In addition, tissue samples from brain and all the
anatomic regions of the gastrointestinal tract (stomach,
small and large intestine) were collected for
histopathological examinations.
The tissue samples were fixed in 10% buffered formalin
and embedded in paraffin routinely.
DIAGNOSIS
Laboratory examinations
Dewaxed 3–5µm thick sections were obtained, and
stained with hematoxylin and eosin (H&E) for
histopathological evaluation
DIAGNOSIS
Results
Fecal samples:
All piglets were positive for TGEV but negative for
porcine rotavirus.
The bacteriological testing was negative for
Escherichia coli and other enteric pathogens.
DIAGNOSIS
Results
Gross and histopathological result:
The necropsy revealed dilation of the intestine,
which contained a small amount of yellowish fluid.
No specific gross lesions were detected in any other
organ.
DIAGNOSIS
Results
Gross and histopathological result:
The histopathological appearance of the small-
intestine examined samples was similar and
characterized by villi fused with denuded tips.
Severe villus atrophy led to extensive epithelial
flattening. It was observed in the middle and lower
small intestine.
DIAGNOSIS
DIAGNOSIS
Results
Gross and histopathological result
The architecture pattern of villi was characterized by
columnar and cuboidal poorly differentiated
enterocytes with mild subepithelial edema.
In some enterocytes, pycnotic nuclei were detected.
No significant lesions were detected either in
stomach or in the large intestine.
DIAGNOSIS
Results
Gross and histopathological result
The examined tissue sections from the brain
revealed diffuse gliosis in the area of pia matter with
mild congestion of the meningeal and parenchymal
vessels and neuronal degeneration accompanied
with neuronophagia.
The above-described lesions were observed mostly
in the parietal and occipital lobe.
DIAGNOSIS
TREATMENT
TREATMENT
• Oral antibiotics in affected piglets to prevent
secondary bacterial enteric infections.
• Oral feed supplements in liquid form based on plant
extracts and herds (phytogenics) to support gut
health and improve nutrient utilization.
• Electrolytes and milk replacers to reduce the
negative effects of severe diarrhea and dehydration.
TREATMENT
• Based on the low mortality rate in piglets, the
common practice of feedback control of TGE (feeding
of sows with TGEV-infected minced intestines) was
not applied to avoid the potential hazards (e.g.,
possible spread of other pathogens to pregnant sows
and throughout the herd)
DISCUSSION
DISCUSSION
• The case report described a TGEV endemic infection
in newborn piglets, characterized by low mortality
rate and medium morbidity rate accompanied by
typical histopathological lesions in middle and lower
small intestine.
• The findings on the lesions of small intestine are in
agreement with those of previous studies.
• Furthermore, coexisting brain lesions were observed,
indicating non-supportive encephalitis, characterized
mainly by diffuse gliosis in the area of pia matter.
DISCUSSION
• This finding suggests that it is possible that TGEV
could also cause brain lesions beyond the known
ones.
• The aforementioned finding also supports the initial
hypothesis on possible effect of TGEV on brain
function, causing vomit due to neural pathway.
• It is known that jejunal enterocytes undergo massive
necrosis within 12–24h after TGEV infection, resulting
in an acute maldigestive and malabsorptive diarrhea
and severe dehydration.
DISCUSSION
• Moreover, other mechanisms such as altered intestinal
sodium transport with accumulation of electrolytes/water
in the intestinal lumen and loss of extravascular protein
are attributed to diarrhea caused by TGEV infection.
• Using different pathways, several viruses have been shown
to be able to penetrate the central nervous system (CNS),
and infect neurons and glial cells.
• The detected brain lesions as degeneration of neurons,
reactivity of the glia, and perivascular inflammatory
reaction are in accordance with the general hallmarks of
viral infection of the CNS.
DISCUSSION
• These lesions, indicating non-supporative
encephalitis, could result from viral infection of CNS
as part of systematic infection.
• Coronaviruses are considered to be neuroinvasive,
neurotropic, and occasionally neurovirulent in various
hosts, including human, cats, pigs, rodents, and fowl,
especially on susceptible individuals.
DISCUSSION
• Hypoglycemia, caused by diarrhea and vomiting in
newborn piglets, is considered the main cause of
death of piglets infected with TGEV.
• As it is established, the brain requires glucose and
oxygen for its energy production.
• The microscopic effects of reduced glucose are
similar to those of oxygen depletion.
DISCUSSION
• Hypoglycemia causes excitotoxicity, which is the term
used for the neuronal death process induced by
massive release of the excitatory amino acid l-
glutamate into the extracellular space after lysis of
neurons from the infarct core.
• So according to the above theory, the hypoglycemia in
this case could be the reason of neuronal degeneration.
• However, more rigorous studies are required to
investigate the pathogenesis of TGEV, especially if the
TGEV has direct or indirect effect on brain function.
DISCUSSION
• In conclusion, this case study reported a TGEV infection
in newborn piglets, characterized by typical
histopathological lesions in small intestine, as well as the
typical pattern of viral brain lesions, suggesting that
TGEV has neurotropic effect.
