Rhabdoviruses Pathogenic Forms for Salmonid Fish, Ethiology

7/30/2019 Rhabdoviruses Pathogenic Forms for Salmonid Fish, Ethiology

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Ali TAVUS


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Rhabdoviruses Pathogenic Forms for

Salmonid Fish

1. Infectious Hematopoietic Necrosis

2. Viral Hemorrhagic Septicemia3. Spring Viremia of Carp


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Infectious Hematopoietic Necrosis

IHNV is transmitted by clinically ill fish and asymptomatic carriers.

This virus is shed in the feces, urine, sexual f luids and external mucus. Transmission

is mainly from fish to fish, primarily by direct contact, but also through the water.

IHNV can survive in water for at least one month, particularly if the water contains

organic material.

This virus can also be spread in contaminated feed.

The gills or the digestive tract have been suggested as the major sites of virus entry,

but recent evidence suggests that IHNV may enter at the base of the fins.

Egg-associated (vertical) transmission also occurs; whether IHNV can be present

inside the egg as well as on the surface is controversial. Invertebrate vectors mayexist


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The clinical signs include abdominal distension, exophthalmia, darkened

skin and pale gills. Long, semi-transparent fecal casts often trail from the

anus. Affected fish are typically lethargic, with bouts of hyperexcitabilityand frenzied, abnormal activity. Petechial hemorrhages commonly occur at

the base of the pectoral fins, the mouth, the skin posterior to the skull above

the lateral line, the muscles near the anus, and the yolk sac in sac fry.

In sac fry, the yolk sac often swells with fluid. In fry less than two months

old, there may be few clinical signs despite a high mortality rate.

Surviving fish often have scoliosis.


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The abdomen, stomach, and intestines often contain white to yellowish

fluid, but food is usually absent from the digestive tract.

The kidney, liver, spleen and heart are typically very pale. Necrosis is

common in the kidney and spleen, and focal necrosis may be noted in

the liver.

Petechiae are often found in the internal organs including the pyloric

caeca, spleen, peritoneum, intestines, and the membranes surrounding

the heart and brain.

Hemorrhages may occur in the kidney, peritoneum and swim bladder.


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Viral Hemorrhagic Septicemia

Viral hemorrhagic septicemia is caused by the viral hemorrhagic

septicemia virus (VHSV or Egtved virus). This virus is a member of the

genusNovirhabdovirus, family Rhabdoviridae.

Currently, the evidence suggests that VHSV contains a single

serotype with three subtypes.

Both marine and freshwater isolates occur. Marine isolates are

indistinguishable from freshwater isolates by routine serology.


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Viral Hemorrhagic Septicemia

VHS has a number of identified isolates (unique genetic types)

grouped in four types; three from Europe and one from North America.

Each appears to have unique effects with specific pathogenicity(virulence) on certain species. The isolate recently found in the Great

Lakes Basin is nearly identical genetically to the VHS strain previously

isolated from the Maritime Region of Canada and has been labeled Type

(isolate) IVb.


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VHSV is shed primarily in the urine and reproductive fluids (ovarian

fluids, sperm). This virus has also been reported in the feces, but

shedding is low. Reservoirs include clinically ill fish and asymptomaticcarriers. Virus carriage seems to be lifelong, but shedding appears to be

intermittent in carriers.

Transmission can occur through the water or by contact. VHSV is

thought to enter the body through the gills or possibly through wounds.

Fish-eating birds can introduce VHSV into areas by acting as

mechanical vectors.


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The incubation period varies with water temperature. Between 1C

(34F) and 12C (54F), the incubation period for European freshwater

VHSV isolates is 1 to 2 weeks at warmer temperatures and 3 to 4 weeksat colder temperatures.


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Affected rainbow trout are usually anorexic and may be either lethargic

or hyperactive. Swimming behavior can also be abnormal. The coloring

is usually darker than normal but the gills are pale due to anemia and

may have petechial hemorrhages. Hemorrhages can also be seen in the

eyes and at the base of the fins, and sometimes on the body surface.

Bilateral or unilateral exophthalmia and ascites may be present. A

neurologic form characterized only by abnormal swimming behavior,such as constant flashing and/or spiraling, can also occur in this

species. Chronic carriers may be asymptomatic.


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Spring Viremia of Carp

Spring viremia of carp is caused by the spring viremia of carp virus

(SVCV), which is also known as Rhabdovirus carpio. This virus is a member

of the family Rhabdoviridae and has been tentatively placed in the genus

Vesiculovirus. SVCV is closely related to pike fry rhabdovirus, and these two

viruses cross-react in some serologic tests.

SVCV strains vary in their pathogenicity. Isolates can be divided into

four genetic groups. Genogroup Ia viruses originate from Asia. Genogroups

Ib and Ic are comprised of isolates from Russia, Moldova and Ukraine.

Genogroup Id mainly contains viruses from the U.K., although a few isolates

in this group are from the former U.S.S.R. SVCV strains from


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SVCV can also be spread by fomites and invertebrate vectors. Infectious

virus can persist in 10C water for more than four weeks and in 4C mud

for at least six weeks. Known vectors include the carp louse Argulusfoliaceus and leech Piscicola geometra, but other aquatic arthropods

might also transmit the virus. Fish-eating birds are also potential

vectors.


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Incubation periods from 7 to 15 days have been reported in

experimental infections


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Fish can carry SVCV with or without symptoms. Fish up to a year old are

most likely to be affected, but illness also occurs in older animals. The

clinical signs are nonspecific. In carp, the most common symptoms include

abdominal distension, exophthalmia, inflammation or edema of the vent

(often with trailing mucoid fecal casts), and petechial hemorrhages of the

skin, gills and eyes. The body is often darkened with pale gills. Diseased fish

tend to gather at the water inlet or sides of the pond, swim and breathe

more slowly than normal, and react sluggishly to stimuli. Loss ofequilibrium, with resting and leaning, are seen in the late stages.

Concurrent bacterial infections (carp-dropsy complex) or parasitic

infections influence the symptoms and mortality rate.


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Post-Mortem Lesions

The body is often darkened with pale gills, and petechial hemorrhages

may be seen in the skin, gills or eyes. The abdominal cavity typically contains

serous fluid, which may be mixed with blood or necrotic material. The muscles

and fat may contain petechial or focal hemorrhages. Similar hemorrhages are

also common on the internal organs, particularly on the walls of the swim (air)

bladder. The intestines are often severely inflamed and dilated, and may contain

necrotic material. The spleen is frequently swollen, with a coarse surface texture.

Other lesions may include degeneration of the gill lamellae, edema of other

internal organs, hepatic necrosis, jaundice, cardiac inf lammation and

pericarditis. In fish that die suddenly, gross lesions may be absent.


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Rhabdoviruses Pathogenic Forms for Salmonid Fish, Ethiology

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