Brief description about CORONAVIRIDAE family

1. F.CORONAVIRIDAE
PRESENTED BY:
ANITTA THOMAS
L-2021-V-46-M

2. INTRODUCTION
Coronaviridae is a family of enveloped, positive-stranded RNA viruses which infect amphibians ,
birds and mammals.

3. HISTORY
• The Coronaviridae were recognized as a new virus family in 1968.
• Torovirus and Coronavirus were recognized as separate genera within the Coronaviridae family
in 1993.
• The 1st reported case of Coronavirus infection in animals was in late 1920.
• First identification of Coronavirus in human was in 1965.

4. CLASSIFICATION

7. Phylogenetic tree of 50 Coronaviruses

8. • The genome of viruses in the family Coronaviridae consists of a single molecule of linear
positive-sense, single-stranded RNA - the largest known nonsegmented RNA viral genomes.
• In infected cells, these viruses all utilize a distinctive “nested set” transcription strategy in which
the expression of genes encoding structural viral proteins is mediated via a nested set of 3’
coterminal subgenomic mRNAs.
• This unique strategy has been recognized by the establishment of the order Nidovirales(from the
Latin nidus, nest).
• It is believed currently that warm-blooded flying vertebrates are the definitive hosts for the
Coronavirus gene pool.
Alpha- and Betacoronavirus - in bats,
Gamma- and Deltacoronavirus - in birds.

9. VIRION PROPERTIES
• They are enveloped,
• Size and shape
Coronaviruses- 80-220 nm in size, pleomorphic although often spherical
Toroviruses and Bafiniviruses - 20-140 nm in size and disc, kidney, or rod-shaped.
• Coronaviruses have distinctive and large (20 nm long) club shaped spikes (peplomers,
composed of trimers of the spike protein).
• The association of the nucleocapsid (N) protein with the genomic RNA forms the helical
nucleocapsid that is surrounded by an icosahedral structure composed of the viral membrane (M)
protein.
• Some coronaviruses also have a second fringe of shorter (5 nm long) spikes (composed of the
hemagglutinin-esterase (HE) protein), a particular characteristics of some Betacoronaviruses.

10. SCHEMATIC STRUCTURE OF PARTICLES OF MEMBERS OF THE ORDER NIDOVIRALES.

11. PROTEINS AND ITS FUNCTIONS
The 16 non structural proteins(nps) are mainly required for transcription and replication of genome,
among which
• nsp1 helps in mRNA degradation
• nsp3 blocks host innate immune response
• nsp14 act as exonuclease
• nsp15 serve as endonuclease.

12. • The major virion proteins of the member viruses of the
subfamilies Coronavirinae and Torovirinae include a
nucleocapsid protein (N, 50-60 kDa, 19 kDa for
Toroviruses) and several envelope proteins:
(1) the spike glycoprotein trimer (S, 180-220 kDa per
monomer);
(2) a triple-spanning transmembrane protein (M, 23-
35 kDa);
(3) a minor transmembrane protein (E, 9-12 kDa),
which together with the M protein is essential for
Coronavirus virion assembly and budding.

13. The 4 structural proteins helps in viral assembly and occurrence of infections.
• S protein - The homotrimer of S protein produce spikes on the surface and are cleaved into
S1&S2 that act as fusion and attachment protein during viral attachment to the host cell.
• M protein- It has 3 transmembrane domain associated with viral envelope that gives shape to
virion and promote membrane curvature.
• E protein- It is responsible for viral assembly , release and pathogenesis, it also act a viroporin
which influence the electrochemical balance.
• N protein- It contains 2 domains (homodimer or homooligomer) , helps in packaging of genome
and antagonize interferon type 1 , that is beneficial for viral replication.
• Some coronaviruses i.e Betacoronavirus encodes some special protein and accessory protein such
as HE with haemaglutinating and estaerase activity and 3a/b,4a/b proteins.

14. • Toroviruses lack a homolog of the Coronavirus E protein, which may explain the structural
differences between the Coronaviruses and Toroviruses.
• Virus neutralizing antibodies generated during natural infections are directed at the surface
glycoproteins of Coronaviruses and Toroviruses - majority being conformational epitopes at the
N-terminal portion of the S protein.
• Cellular immune responses are principally directed toward the S and N proteins.

16. VIRUS REPLICATION
ATTACHMENT AND ENTRY
• The host spectrum/tropism of individual Coronaviruses appears to be largely determined by
the S protein - which mediate receptor binding and virus cell fusion (in plasma membrane /
endosomes).
• Virus replication and transcription takes place within an extensive membranous network of virus-
modified endoplasmic reticulum-derived vesicles.
• Individual Coronaviruses utilize a variety of cellular proteins as receptors.
• Aminopeptidase N (APN or CD13) serves as a receptor for several Alphacoronaviruses.

17. • SARS Coronavirus and human Coronavirus NL63 utilize angiotensin converting enzyme 2
(ACE2).
• MERS coronavirus utilizes dipeptidyl-peptidase 4 (DPP4 or CD26).
• Some strains of mouse hepatitis virus utilizes carcinoembryonic antigen related cell adhesion
molecule 1 (CEACAM-1).
• Other Betacoronaviruses utilize sialic acids as a primary receptor.
• In addition to receptor binding, the activation of virus fusion via the action of host cell-specific
proteases that cleave spike is likely to be a powerful means of regulating Coronavirus infection
and host- or tissue-tropism.

18. VIRUS REPLICATION AND TRANSCRIPTION
• Takes place within an extensive membranous network of virus-modified endoplasmic reticulum-
derived vesicles.
• The strategy of viral replication and transcription of the Coronavirus genome is complex.
• The viral RNA serves as mRNA for synthesis of the RNA dependent RNA polymerase (RdRp).
• The two large 5’-most open reading frames, ORF1a and ORF1b ( 20 kb in total size) encoding
the subunits of the polymerase are translated, the larger via ribosomal frameshifting -as a single
polyprotein (pp1a or pp1ab) that is then cleaved by virus-encoded proteases found within the
polyprotein, resulting in the production of mature products - nsp1 to nsp16.

20. • These proteins then assemble to form the active replicase transcriptase complex, comprising
the RNA polymerase (nsp12) and accessory proteins, including a 3’-5’ exonuclease that imparts
some degree of “proof reading” function during replication.
• Such proof reading activity is thought to be important in maintaining the integrity of such large
RNA genomes.
• The viral polymerase is used to synthesize full-length negative-sense (complementary) RNA by
copying the genome starting at the 3’ end.
• The antigenome is then copied back into full-length positive-sense genomic RNA.
• The generation of full-length genomic RNA is done utilizing the replicase activity of the viral
RdRp.

21. • The RdRp can also synthesize a nested set of RNAs with different sizes that are generated by a
discontinuous synthesis of negative-sense RNAs.
• This is done using the transcriptase activity of the RdRp.
• The RdRp synthesizes negative-sense RNA by starting to copy at the 3’ end of the genome, it then
recognizes internal regulatory sequences, the transcriptional regulatory sequences (TRSs)
found upstream of each ORF, where it pauses and translocates to the 5’ end of the genome, guided
by sequence complementarity.
• The RdRp then extends the nascent negative-sense RNA by copying the leader sequence found at
the genome’s 5’ end.
• These negative sense template RNAs, sharing both 5’ and 3’ ends, are copied into positive-sense
subgenomic mRNAs which then allow expression of viral genes downstream of the replicase.

22. • The template switching employed during transcription is at the heart of the RNA
recombination that is a hallmark of Coronavirus replication.
• The accumulation of point mutations as a result of polymerase errors (infidelity) during
transcription (Genetic drift), genetic recombination occurs at high frequency between the
genomes of different but related Coronaviruses during coinfection situations.
• Recombination between Coronaviruses is a direct result of the discontinuous transcription
strategy employed by the viral polymerase, and the presence of transcriptional regulatory
sequences in the viral genome.
• Such recombination is likely to be an important mechanism for the generation of the genetic
diversity seen with these viruses in nature, and provides a constant potential source of new viruses
with novel phenotypic properties, such as host range, tissue tropism, and virulence.

23. SUBFAMILY TOROVIRINAE
• The transcription and replication apparently are similar to those of coronaviruses, except that
there are no common 5’ leader sequences on the mRNAs of viruses in the genus Torovirus.
• As occurs during replication of Coronaviruses, subgenomic negative-sense RNAs complementary
to the nested set of mRNAs are also present in Torovirus -infected cells.
• The fact that these subgenomic RNAs contain 5’ -and 3’ -terminal sequences that are identical to
those of genomic RNA implies that they may function as replicons.
• Viruses in the genus Bafinivirus use the same transcriptional strategy as the coronaviruses and
produce their replicase polyproteins from the virus genome and the three structural proteins from
a nested set of 3’ -coterminal subgenomic mRNAs, each having a common 5’ leader sequence
identical to that of the virus genome.

24. ASSEMBLY AND RELEASE
• Following replication and sub-genomic RNA synthesis, the viral structural proteins, S, E, and M
are translated and inserted into the endoplasmic reticulum (ER).
• These proteins move along the secretory pathway into the endoplasmic reticulum-Golgi
intermediate compartment (ERGIC)
• There, viral genomes encapsidated by N protein bud into membranes of the ERGIC containing
viral structural proteins, forming mature virions.
• Virions are transported to the cell surface in vesicles and released by exocytosis.
• After their release, many of the mature enveloped virions remain adherent to the outside of the
cell.

25. CORONAVIRUS REPLICATION

26. SUBFAMILY CORONAVIRINAE
GENUS ALPHACORONAVIRUS
FELINE CORONAVIRUS (FELINE INFECTIOUS
PERITONITIS VIRUS)
• Feline infectious peritonitis (FIP) was first described in the 1960s as a systemic and often fatal
disease of cats.
• The pathogenesis of feline infectious peritonitis is complex and not fully characterized.
• The sporadic occurrence of feline infectious peritonitis is proposed to be the result of mutations of
the enteric Coronavirus during natural infection of cats, resulting in the emergence of a virus with
an acquired tropism for macrophages.

27. • Two distinct serotypes of the virus have been identified, both being able to cause feline
infectious peritonitis.
Serotype I - majority.
Serotype II - relatively rare.
• Serotype II feline infectious peritonitis viruses grow well in cell culture and utilize amino-
peptidase-n (APN) as a receptor. In contrast, serotype I viruses are very difficult to culture, and
appear to use a distinct and currently unidentified receptor.
• Both virus types can cause the 2 clinical forms of feline infectious peritonitis
The “wet” form ( with abdominal effusion )
The “dry” form (without abdominal effusion).

28. CLINICAL FEATURES AND EPIDEMIOLOGY
• Feline infectious peritonitis is a common progressive, debilitating and lethal disease of domestic
and wild members of the family Felidae.
• Disease typically occurs in young or very old cats, or in the context of immune suppression.
• The initial clinical signs are vague, and affected cats present with anorexia, chronic fever, malaise,
and weight loss.
• Ocular and/or neurological manifestations occur in some individuals.
• In the classical wet or effusive form - these signs are accompanied by progressive abdominal
distention from the accumulation of a highly viscous fluid in the peritoneal cavity and rapid
disease progression, with death typically within weeks to months.

29. • The dry or non-effusive form of the disease- little or no peritoneal exudate, is more slowly
progressive.
• The wet and dry forms of feline infectious peritonitis are different manifestations of the same
infection, and both forms of the disease are characterized by foci of pyogranulomatous
inflammation in several organs.
• A kitten suckling a seropositive queen - persistent viral infection of the gut with chronic fecal
shedding is established. Virus and antibodies coexist in the kitten. The animal may remain
healthy, but becomes susceptible to development of feline infectious peritonitis should it become
stressed or immunosuppressed.

31. PATHOGENESIS AND PATHOLOGY
• The key initiating pathogenic event is the productive infection of monocytes and macrophages
by genetic variants (mutants) of the original enteric Coronavirus.
• Avirulent strains are also less able to sustain virus replication and spread between macrophages.
• Mutations within the spike (S) - alter the tropism of the ubiquitous avirulent feline enteric
Coronavirus to macrophages, which then allows the virus to spread and ultimately to cause feline
infectious peritonitis.
• The lesions - centered on small blood vessels, and vascular injury and leakage are central to the
pathogenesis of the wet form of the disease.
• Perivascular clusters of virus-infected macrophages are characteristically present in the tissues
of cats with both the wet and dry forms of feline infectious peritonitis.

32. • Humoral immunity is not protective, and may actually enhance disease progression.
• Antibody-dependent enhancement of infection of macrophages is apparently mediated by
neutralizing antibodies to the S protein, making vaccine development problematic.
• The gross lesions (one of the two forms)
The wet form -presence of variable quantities of thick, viscous, clear yellow peritoneal exudate,
and the presence of extensive fibrinous plaque with numerous discrete gray-white nodules in the
omentum and on the serosal surface of the liver, spleen, intestines, and kidneys.

33. • Microscopically, these nodules are composed of
aggregates of macrophages and other inflammatory
cells (granulomas or pyogranulomas) that
characteristically are centered on blood vessels,
sometimes with necrosis of the wall of involved
vessels. These lesions can occur in many tissues, but
omentum and peritoneal serosa, liver, kidney, lung and
pleura, pericardium, meninges, brain, and uvea are
common sites.

34. • The dry form - lesions and pathogenesis similar, but without the fibrinous polyserositis that
characterizes the wet form, and discrete pyogranulomas form nodular masses within the
parenchyma of affected organs.
• It is unknown what determines the form of feline infectious peritonitis that develops in an
individual cat
• Individual virus strains can cause either form in different animals and both forms may be present
in a single cat.

35. DIAGNOSIS
• Effusive form : Detection of viral RNA in a sample of the effusion by RT-PCR
Measure the total protein in the effusion: if it is less than 35g/L, FIP is extremely unlikely.
Albumin to globulin ratio in the effusion: if it is over 0.8, FIP is not present if it is less than 0.4,
FIP may occur.
• Non-effusive : History, Clinical signs ,biochemistry: hypergammaglobulinaemia; raised bilirubin
without liver enzymes being raised.
• Hematology: lymphopenia; non-regenerative-usually mild-anaemia.
• Serology: the infected cat has a high antibody titre to FCoV but some times infected cats are
seronegative.

36. IMMUNITY, PREVENTION, AND CONTROL
• Feline infectious peritonitis is not controlled easily; control requires the elimination of the virus
from the local environment,
• Requires a high level of hygiene, strict quarantine, and immunoprophylactic measures. Because
kittens acquire the infection from their queens, early weaning programs have also been used to
interrupt virus transmission.
• The only commercially available feline infectious peritonitis vaccine contains a temperature-
sensitive mutant virus, based on a serotype II virus.
• Vaccination of infected, seropositive adult cats is not effective.
• Treatment : Anti inflammatory drug , immunostimulants and antiviral drugs can be used.

37. VACCINES
cats 16 weeks of age
or older

38. CANINE CORONA VIRUS
• Canine coronavirus is an alphacoronavirus usually produces a mild - identified in 1971.
• The disease commonly occurs in association with canine parvovirus infection, which causes a
more severe and sometimes fatal diarrhea.
• The virus commonly infects pups and is probably worldwide in distribution.
• Confirmed by laboratory-based procedures. Such as visualization of virus by electron microscopy
or may be isolated in primary canine cell culture.
• Detection of antibody in the sera of pups is of limited value because it may be of maternal origin.
• Inactivated vaccine is available for the control of canine coronavirus diarrhea.

39. Vaccination: healthy dogs 6 wks and older

40. TRANSMISSIBLE GASTROENTERITIS
VIRUS
• There are four distinct corona virus disease patterns in swine, referred to as (1) vomiting and
wasting disease, (2) porcine epidemic diarrhea, (3) transmissible gastroenteritis, and (4)
respiratory disease.
• TGE is a highly contagious enteric disease of swine that occurs throughout much of the world.
• It is an acute, rapidly spreading, disease of swine of all ages, characterized by diarrhea and
vomiting.
• High mortality in piglets under two weeks of age is common.

41. CLINICAL FEATURES AND EPIDEMIOLOGY
• Most severe in very young piglets, and include vomiting, profuse watery yellow diarrhea, rapid
weight loss, and dehydration.
• Seronegative neonates succumb within a few days of infection with highly virulent strains,
whereas death is uncommon in pigs infected after 2-3 weeks of age.
• Infections of adult swine typically are asymptomatic.
• Spread among farms occurs with the introduction of pigs excreting the virus or by mechanical
vectors (fomites) such as contaminated vehicles, clothing, instruments, etc.

42. Profuse watery diarrhea Dehydration

43. PATHOGENESIS AND PATHOLOGY
• Incubation period of 18-72 hours.
• Virus enters the body by ingestion (fecal-oral transmission).
• Reasons for the susceptibility of very young piglets:
(1) their gastric secretions are less acidic
(2) renewal of enterocytes lining the intestinal villi from progenitor cells in the intestinal crypts is
less rapid than in older pigs;
(3) the neonatal immune system is naive and not fully mature;
(4) neonates are especially vulnerable to the electrolyte and fluid derangements that result from the
maldigestion and severe malabsorption diarrhea.

44. • The virus selectively infects and destroys the mature enterocytes lining the small intestinal villi.
• Results in profound shortening and blunting of villi, with consequent loss of the mucosal
absorptive area .
• This leads to maldigestion because of the loss of critical digestive enzymes such as lactase and
other disaccharidases, normally present in the microvillus brush border of villus enterocytes, that
are responsible for digestion of milk.
• The consequence - acidosis, and severe dehydration.
• Intestinal crypt epithelial cells remain uninfected, so recovery of the integrity and function of villi
is rapid if the animal survives the infection.
• the proliferation of progenitor enterocytes in the crypts also increases intestinal secretion of fluid
and electrolytes, which further exacerbates the diarrhea and metabolic pertubations.

45. Viral infection and destruction of enterocytes lining
small intestinal villi, leading to malabsorption
diarrhea.
(A) Causative virus (arrow).
(B) Small intestine of normal piglet
(C) Piglet with transmissible gastroenteritis.
(D) Selective viral infection of enterocytes
lining the intestinal villi.

46. DIAGNOSIS
• Mucosal impression smears or cryostat sections of intestine from neonatal piglets with acute
disease can be stained by immunofluorescence or immunoperoxidase procedures.
• Antigen capture enzyme-linked immunosorbent assay (ELISA) - in the feces of infected pigs.
• Virus isolation can be done in porcine kidney, thyroid, or testicle cells.
• None of these assays definitively differentiates TGE and porcine respiratory coronavirus
infections.

47. IMMUNITY, PREVENTION, AND CONTROL
• Oral vaccines have not proven highly
effective.
• Maternal IgA antibodies, passed to piglets in
colostrum and milk, provide protection
against infection.
• Strict sanitation and management practices. 1st : 2ml 5-7 wks IM
before delivery
2nd : 2ml 2-3 wks IM
before delivery.
Pregnant sow: 4ml 20-30
days before birth

48. PORCINE EPIDEMIC DIARRHEA VIRUS
• Clinically similar to transmissible gastroenteritis, but spreads more slowly. The virus that causes
this disease is unrelated to the other porcine corona viruses.
• The main clinical sign in piglets is watery diarrhea, sometimes preceded by vomiting.
• In adult swine the infection may remain asymptomatic or may be limited to depression, anorexia,
and vomiting.
• The mortality rate in piglets is usually about 50% but may be as high as 90%. Older pigs recover
after about 1 week of illness.

49. DIAGNOSIS
• A may be confirmed by the isolation of virus in primary porcine cell culture
• Demonstration of antibodies in convalescent swine.
• Vaccines are not available.

50. PORCINE RESPIRATORY CORONAVIRUS
• The respiratory variant of transmissible gastroenteritis virus.
• The virus is a spike protein (S gene) deletion mutant that has lost its enteric tropism.
• Instead acquired a respiratory tropism and transmission pattern
CLINICAL FEATURES AND EPIDEMIOLOGY
• Mild fever with variable degrees of dyspnea, polypnea, and anorexia.
• Spreading long distances by airborne respiratory transmission or directly by contact.

51. PATHOGENESIS AND PATHOLOGY
• The large 5’ region deletion in the spike gene accounts for the reduced virulence and altered
tropism of this virus.
• Spread by respiratory droplets and aerosols and, after infection.
• Replicates in the tonsils, the mucosal epithelium of the nasal mucosa and airways of the lungs,
and in both type I and II pneumocytes in alveoli.
• Virus-induced inflammation and necrosis in the terminal airways and airspaces manifest as
bronchointerstitial pneumonia that can affect 5-60% of the lung, even in subclinically infected
pigs.
• The severity of clinical signs and lesions vary, but infection is subclinical in many infected herds.

52. DIAGNOSIS
• Detected readily in nasal swabs.
• Two related viruses are only distinguished by virus-specific RT-PCR assays or highly specific
competitive ELISA.
• The virus also can be isolated and grown in pig kidney or testicle cells.
IMMUNITY, PREVENTION, AND CONTROL
• No vaccines for prevention.

53. PORCINE HEMAGGLUTINATING
ENCEPHALOMYELITIS VIRUS
• In piglets less than 2 weeks of age.
• Characterized by anorexia, hyperesthesia, muscle tremors, paddling of the legs, vomiting, and
depression, often leading to emaciation and death.
• In contrast to transmissible gastroenteritis, diarrhea is not common.
• Mortality in young piglets is high; older animals often survive but remain permanently stunted.

54. PATHOGENESIS
• The virus multiplies first in the nasal mucosa, tonsils, lung, and small intestine and then spreads to
the central nervous system via peripheral nerves.
• In the central nervous system, virus is first detected in the sensory nuclei of the trigeminal and
vagus nerves, with subsequent spread to the brain stem, cerebrum, and cerebellum.
• One characteristic clinical sign, vomiting, is due to virus replication in the ganglion distale vagi;
and wasting, is due to neurologic disturbance of the vomition center.
• Severe, unremitting vomiting leads to malnutrition

55. DIAGNOSIS, PREVENTION AND CONTROL
• A clinical is confirmed by the isolation of virus in primary porcine cell culture; growth of the
virus is detected by haemagglutination.
• No vaccines are available,
• Good husbandry is essential for the prevention and control of the disease

56. BOVINE CORONAVIRUS ENTERITIS
• Second to rotaviruses as the major cause of diarrhea in young calves.
• Corona-viruses were first reported as a cause of diarrhea in calves in the United States in 1973,
• Recognized worldwide.

57. PATHOGENESIS
• The pathogenesis is similar to that of rotavirus diarrhea.
• Disease is seen most commonly in calves at about 1 week of age, the time when antibody in the
dam's milk starts to wane and exposure is maximal.
• The diarrhea usually lasts for 4 or 5 days.
• The destruction of the absorptive cells of the intestinal epithelium of the small intestine and, to a
lesser extent, the large intestine leads to the rapid loss of water and electrolytes.
• Glucose and lactose metabolism are affected; hypoglycemia, lactic acidosis, and hypervolemia
can lead to acute shock, cardiac failure, and death.

58. DIAGNOSIS
• Initially, diagnosis was based on the detection of virus by electron microscopy, but subsequently
the addition of trypsin to bovine cell culture medium was shown to facilitate the isolation of virus.
• Bovine cells and human HRT-18 cells are used for primary isolation. Viral growth may be
recognized by hemadsorption.

59. PREVENTION AND CONTROL
• Available vaccines are not effective because they do not appear to contain sufficient antigenic
mass and they evoke protection at the time of maximum risk.
• One alternative to vaccinating calves is to immunize the dam, thereby promoting elevated
antibody levels in the colostrum.
• Another alternative is to feed calves colostrum and milk from hyperimmunized cows used as
donors.

60. INFECTIOUS BRONCHITIS VIRUS (IBV)
• An acute, highly contagious respiratory disease of chickens.
• All ages infected; particularly a problem in laying flocks.
• Chicks - growth suppression & predisposition to other diseases.
• Hens - variable production loss and affects egg quality.
• Turkeys resistant.
• Various serotype of the virus are: Massachusetts, Connecticut(Affiity for respiratory tract )T,
Gray, Holte( Nephrotoxic)

61. PATHOGENESISS
• IB virus initially infects and replicates in upper respiratory tract causing the loss of protective
lining the sinuses and trachea.
• After causing viremia, the virus can be detected in kidneys, reproductive tract, and caecal tonsils.

62. CLINICAL FEATURES
This disease has 4 form
• The incubation period is 18–48 hours.
• Respiratory form: In chicks 1–4 weeks of age, virulent virus strains produce severe respiratory
disease, with gasping, coughing, tracheal rales, sneezing, nasal exudate, wet eyes, respiratory
distress, and swollen sinuses.
• Genital form :Infection of young female chicks may result in permanent hypoplasia of the
oviduct that is evident later in life as reduced egg production.
• Egg-laying chickens usually present with reproductive tract involvement that is manifest as a
decline or cessation in egg production including abnormal egg that lack calcified shell, thin
shells egg , and shells with stipples, distortions,
• Nephritic form: Acutely infected birds, the kidneys can be pale and swollen, with urates
distending the ureters.
• Gastrointenstinal form: some birds

63. • Other clinical signs - restless and huddled
together, difficult in breathing, gasping,
coughing, sneezing, tracheal rales, nasal
discharge, wet eye and swollen sinus, ruffled
feathers, morbidity up to 100%.
• Facial swelling may also occur occasionally,
particularly with concurrent bacterial
infection of the sinuses.
• Decrease of feed intake and conversion, loss
of body weight
• increased water intake, wet droppings,
depression, lethargy and poor growth in
broilers
IBV- infected egg abnormalities

64. POSTMORTEM LESIONS:
Gross:
• The most frequent finding is mucosal thickening, with serous or catarrhal exudate in the nasal
passages, trachea, bronchi, and airsacs.
• Very young chicks, the main bronchi may be blocked with caseous yellow casts.
• Pneumonia and conjunctivitis.
• In laying birds, ova can be congested and sometimes ruptured, with free yolk in the abdominal
cavity.
Microscopic:
• Desquamation of respiratory epithelium, edema, epithelial hyperplasia,
• mononuclear cell infiltration of the submucosa, and regeneration.

65. Airsacculitis Exudate in trachea

66. DIAGNOSIS
• History of fast spreading respiratory disease
• ELISA - uses Mass. antigen but get cross reaction with other serotypes.
• HI - IBV is treated with neuraminidase enzyme before testing because IBV is not naturally
hemagglutinating.
• VN - rises in titer between paired serum samples (2 wks. apart)
• Agar-gel precipitation test (AGPT)
• Direct immunofluorescence staining of tracheal tissue smears can be done.
• Identification of IBV serotype - PCR, monoclonal antibody test, etc.
• Detection of virus genome (RT-PCR)

67. • For virus isolation , 9-11 day old
embryonated eggs are inoculated via the
allantoic sac route.
• Changes in main blood vessels in the
chorioallantoic membrane and embryo
stunting, curling, clubbing of down
suggestive of the presence of a
coronavirus.
IBV-infected
embryo
Normal
embryo

68. PREVENTION AND CONTROL
• Establish and enforce a biosecurity program.
• Vaccination - complete prevention of IB is difficult because of variation of field strains and
the ability of the virus to change. There is little cross protection between serotypes.
LIVE - Monovalent - usually Mass.
• Bivalent - Mass. & Connecticut
• Other attenuated strains such as Holland an dArk. 99 are used as vaccines.
KILLED - used in breeders and layer pullets to prevent production losses and produce
consistently high antibody titers.

69. • The first vaccination is typically
given in the hatchery when birds are 1
day old, and booster vaccination is
given at 10–18 days.
• Layers or breeders, attenuated
vaccines are used for priming,
followed by killed oil-adjuvanted
booster vaccines.

70. TURKEY COMB DISEASE
• First recognized in turkeys in the United States in 1951 and were associated with various enteric
disease syndromes, variously termed “blue comb disease,” “mud fever,” “transmissible
enteritis,” and “coronaviral enteritis.”
• The onset is characterized by loss of appetite, watery diarrhea, dehydration, hypothermia, weight
loss, and depression.
• The duodenum and jejunum are pale and flaccid, and the ceca filled with frothy content cloacal
bursa is atrophic.
• Only palliative treatment is possible .