Monday, 1 May 2017
Friday, 15 July 2016
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| It's a team effort- The Researchers: Dr. L.W Njagi (PI), myself and fellow investigator Dr. Wahome inoculating chicks for virus amplification. |
Thursday, 26 May 2016
CANINE INFLUENZA VIRUS
Canine Influenza virus (CIV)
Domestic dogs have for
centuries been considered refractory to infection by influenza A viruses. But following reports of transmission of
influenza virus H3N8 sub-type from horses to dogs in the state of Florida/USA in
2004, this theory has so far been challenged. H3N8 influenza A sub-type which
usually afflicts horses, has been associated with outbreaks of a fatal
respiratory disease in Racing Greyhound dogs (fatality rate of 36%). This cross species transmission of H3N8 virus has been related to the proximity of Race-horses
to racing Greyhounds which enabled this virus (H3N8) to infect the dogs.
Most of these dog
infections are mild and are followed by a prompt clinical improvement. H3N8 Canine Influenza Virus (CIV) infections
spread among canine population (both racing greyhounds and pet dogs) of the
USA, without association with outbreaks of equine influenza, supporting a
possible horizontal transmission among dogs.
H3N8 CIV isolates now form
a single group of viruses that are molecularly and epidemiologically distinct
from currently circulating H3N8 equine influenza virus (EIV) in the USA. As the H3N8 CIV is a relatively novel pathogen in
the canine population, dogs lack natural immunity against the virus.
All dogs, regardless breed or age, are therefore susceptible to H3N8 CIV infection and the virus has been shown to rapidly spread within dog populations.
All dogs, regardless breed or age, are therefore susceptible to H3N8 CIV infection and the virus has been shown to rapidly spread within dog populations.
About 80% of infected
animals develop clinical signs upon infection whereas 20-25% develops
subclinical infection, but also shed and transmit the virus. Outbreaks can
occur when clinically normal carriers come into contact with a naïve
population.
The highest risk for
exposure to CIV occurs in communal facilities where dogs are housed and/or
placed in the following conditions:
·
high population density;
·
Indoor (closed-air) environments, such
as racing kennels, dog shows, agility events, animal shelters, kennel boarding
and training facilities, veterinary clinics, pet day-care centers, pet stores,
and pet grooming salons.
Additionally, stressful
situations, - such as travel, prolonged endurance exercise in severe weather,
and exposure to harsh terrain -, might increase the risk for influenza
infection in dogs.
Currently, canine
influenza (CI) caused by H3N8 is considered an endemic disease in metropolitan
areas of the North-eastern and Western regions of the USA, and has been confirmed in Korea, China and Thailand resulting in high morbidity (80%) and low mortality (1-5%) in the dog population. CIV infection
is not considered a seasonal flu and dog infections can occur year-round.
CIV is transmitted by direct contact, through aerosols generated by coughing and sneezing and by
indirect contact through fomites contaminated with respiratory secretions and
by people handling septic animals.
The incubation period
is usually less than five days, with the highest shedding occurring before the development
of clinical signs. CIV replicates in the respiratory epithelium, causing
tracheitis, bronchitis and bronchiolitis. As a result, the defense mechanisms
of the respiratory tract become severely compromised, predisposing to secondary
infections by bacteria or mycoplasma.
Dogs of all ages seem
to be equally susceptible to CIV-associate pneumonia.
Most dogs develop a mild form of the disease, characterized by persistent fever for one to four days (>39.4°C), depression, apathy, anorexia, sneezing, nasal and ocular discharge.
The cough is usually non-productive and persists for 10 to 30 days. Most dogs eradicate the infection and recover clinically within two weeks.
Most dogs develop a mild form of the disease, characterized by persistent fever for one to four days (>39.4°C), depression, apathy, anorexia, sneezing, nasal and ocular discharge.
The cough is usually non-productive and persists for 10 to 30 days. Most dogs eradicate the infection and recover clinically within two weeks.
The clinical
presentation of CIV infection is similar to that observed in “kennel cough” or
infectious tracheobronchitis. CI diagnosis therefore requires laboratory
confirmation, usually virus isolation, RT-PCR and/or testing of paired serum
samples by hemagglutination inhibition (HI).
Treatment consists
mainly of supportive care, including antibiotics for secondary bacterial
infections and hydration.
Preventive measures
include isolation of sick dogs and decontamination of premises with Quaternary
ammonium compounds or sodium hypochlorite. Contact of horses with dogs should be avoided
during outbreaks of equine influenza.
Vaccination of dogs against H3N8 CIV has been authorized in the USA since 2009, but vaccination should be restricted to animals that travel to high-risk areas experiencing canine or equine influenza. Vaccination significantly reduces virus shedding and the severity and duration of clinical disease, including the incidence and severity of lung damage.
Vaccination of dogs against H3N8 CIV has been authorized in the USA since 2009, but vaccination should be restricted to animals that travel to high-risk areas experiencing canine or equine influenza. Vaccination significantly reduces virus shedding and the severity and duration of clinical disease, including the incidence and severity of lung damage.
By:
Dr. Moses Bwana
Post-grad Student at the University of Nairobi
Department Pathology,Microbiology and Parasitology
Monday, 21 March 2016
Hepatitis E Virus
Hepatitis E virus (HEV) is an emerging zoonotic virus
of pigs. It has now been reclassified as the only member of the genus Hepevirus,
family Hepeviridae. The viral particle is composed of a non-enveloped
capsid which encloses a single-stranded positive sense RNA genome. Four main genotypes (HEV 1-4) are identified; two of
them circulate among pigs and humans.
HEV was first detected in
pigs in 1997 in United States. The first swine HEV strains shared about 97%
percent similarity with concurrent strains isolated in humans, showing the zoonotic
potential of the virus.
Virtually all swine-producing countries have already
reported the circulation of swine HEV. Although swine infection is spread
worldwide, the cases of human HEV induced hepatitis are far more common in
developing countries, indicating that poor levels of sanitation and inadequate
disposal of swine manure may have an association with the epidemiology of human
infection.
The disease caused by HEV in humans have some similarities
with that caused by the Hepatitis A virus (HAV), including the fecal-oral route
of transmission and the absence of chronification.
The mortality rate is remarkably higher in pregnant
women, where HEV can cause the death
of up to 20% of patients, while in the non-pregnant population HEV induces up to 4% of deaths.
of up to 20% of patients, while in the non-pregnant population HEV induces up to 4% of deaths.
Although HEV seems to be an important agent of human
liver disease, the infection by swine HEV in pigs is subclinical. After infection, pigs become viremic and shed the
virus on theirs feces from 8 days for up to 12 weeks. The immunity raised by
the infection is long lasting and a prior infection with swine HEV prevents the
onset of viremia and fecal shedding of the virus is also diminished in immune animals.
Viruses from all 4 genotypes cause disease in humans,
whereas only genotypes 3 and 4 are found in pigs. Genotype
1 is mainly found in Asia and Africa, during HEV epidemics in humans; genotype
2 was firstly reported in Mexico and was further reported as an endemic virus
in parts of Africa. These genotypes are restricted
to humans. Genotype 3 is worldwide
distributed and has been causing infection in both humans and swines. This genotype
is often associated to epidemics of HEV liver disease in humans in South America
and is also found on swine in this same region. Genotype
3 HEV strains were also found in many other animal reservoirs including wild
boar, rabbits, rats, deer and mongoose. Similarly,
genotype 4 HEV was detected in humans and pigs, as well in wild boars.
The ubiquitous nature
of HEV infection in pigs suggests that contamination of meat products by HEV
and viscera can be quite frequent. Sporadic cases
of acute hepatitis E have been associated with the consumption of raw pork
liver and under-cooked contaminated pork or grilled meats.
The prevalence of HEV in pigs fed on kitchen
residues is higher than in those fed on complete feed, indicating that indirect
contact with infected humans is also a source of infection for pigs. Veterinarians and swine handlers are at higher
risk of infection than the general population.
HEV has the ability to contaminate water bodies and
be transmitted by water. Contaminated water therefore constitutes a major source of HEV infection in humans and the
reason of ubiquity and perpetuation of the infection in pigs.
Outbreaks of HEV in humans tend to be more common in
regions where conditions of water and sewage treatment are poor. HEV has been found
contaminating the effluents of slaughterhouses and the virus is often found in swine
manure storage facilities.
Control measures to avoid the contamination of the
environment, including better management practices to deal with swine manure,
proper cooking of pork liver and development of swine HEV vaccines.
Dr.
Moses Bwana
Post-grad at the University of Nairobi (Veterinary Applied
Microbiology [Virology Option])
Faculty of Veterinary Medicine
Monday, 29 February 2016
CANINE PARVOVIRUS
Canine Parvovirus (CPV)
infection is a relatively new disease that appeared for the first time in dogs
in 1978. Because of the severity of the disease and its rapid spread through
the canine population, CPV has aroused a great deal of public interest. The virus
that causes this disease is very similar to feline panleukopenia (feline
distemper) and the two diseases are almost identical.
Parvo is caused by
Canine Parvovirus type 2 which is a small non-enveloped single stranded DNA
virus belonging to the genus Parvovirus,
subfamily Parvovirinae and family the
Parvoviridae family. CPV-2 replicates in dividing cells especially
intestinal, lymphoid, bone marrow and fetal tissues and is severely pathogenic.
This virus is known simply as canine parvovirus or CPV.
Three slightly
different strains of canine parvovirus, named CPV-2a, CPV-2b and CPV-2c, are
recognized. They cause the same disease and vaccines give protection against all
the variants. These current variants have different antigenic structures,
increased pathogenicity, and a shorter incubation period (4-5 days vs 5-8) than
CPV-2. These variants also replicate efficiently in cats.
Important
clinical features of the virus
Parvoviruses- resistant
to inactivation; can remain infectious outside the host > 5 months.
CPV stable in the environment and is resistant to the effects of heat, detergents, alcohol, and many disinfectants.
CPV-2 hemagglutinates RBCs from a number of species so hemagglutination assays are
useful for diagnosis.
CPV stable in the environment and is resistant to the effects of heat, detergents, alcohol, and many disinfectants.
CPV-2 hemagglutinates RBCs from a number of species so hemagglutination assays are
useful for diagnosis.
Host range and Epidemiology
Almost all Canidae are susceptible. Within domestic dog populations, Dobermans
pinschers, Rottweilers, English Springer Spaniels, American Pit bull terriers and German Shepherds are at higher risk of severe illness.
Almost all Canidae are susceptible. Within domestic dog populations, Dobermans
pinschers, Rottweilers, English Springer Spaniels, American Pit bull terriers and German Shepherds are at higher risk of severe illness.
Parvo may affect dogs
of all ages, but is most common in dogs less than one year of age. Young
puppies less than five months of age
are usually the most severely affected, and the most difficult to treat.
Age and immunity
determine whether CPV infection results in myocardial
disease or enteritis. Cardiac myocyte replication is sufficient enough only to
support virus until 2 weeks of age. Although myocarditis is seen in pups at 6
to 8 weeks of age, it is the result of infection
several weeks earlier. Enteritis is commonly seen in pups 6 to 16 weeks of age.
Intact male dogs seem more predisposed to infection than intact females. Unvaccinated dogs - about 13 times more likely to become infected than vaccinated dogs.
several weeks earlier. Enteritis is commonly seen in pups 6 to 16 weeks of age.
Intact male dogs seem more predisposed to infection than intact females. Unvaccinated dogs - about 13 times more likely to become infected than vaccinated dogs.
Concurrent infection
with other gastrointestinal pathogens (Giardia, hookworms and
roundworms, coronavirus) may exacerbate the severity of CPV infection.
roundworms, coronavirus) may exacerbate the severity of CPV infection.
Stress of overcrowding,
poor nutrition, and age at infection can dictate the outcome of infection.
Fecal-oral
route: A vast amount of virus is shed in the faeces of
clinically infected dogs.
However, the persistence of virus in the environment is thought to be more important than
chronic carriers in perpetuating disease – not clear if carrier state exists?
Susceptible dogs become infected by ingesting the virus. Active shedding of virus occurs up to the first 2 weeks post inoculation. Generally, dogs that recover from infection do not transmit disease to susceptible kennel mates.
However, the persistence of virus in the environment is thought to be more important than
chronic carriers in perpetuating disease – not clear if carrier state exists?
Susceptible dogs become infected by ingesting the virus. Active shedding of virus occurs up to the first 2 weeks post inoculation. Generally, dogs that recover from infection do not transmit disease to susceptible kennel mates.
Due to its stability, the
virus is easily transmitted via the hair or feet of infected dogs, contaminated
shoes, clothes, and other objects or areas contaminated by infected faeces.
The clinical signs and
symptoms of CPV disease can vary, but generally they include severe vomiting
and diarrhea. The diarrhea often has a very strong smell, may contain lots of
mucus and may or may not contain blood. Additionally, affected dogs often
exhibit a lack of appetite, marked listlessness and depression, and fever. It
is important to note that many dogs may not show every clinical sign, but vomiting
and diarrhea are the most common and consistent signs; vomiting usually begins
first.
Diagnosis
The clinical signs and symptoms of CPV are variable and dependent on age, immunity, co-pathogens (parasites, enteric bacteria, viruses) and infective dose of the virus. These signs can mimic many other diseases that cause vomiting and diarrhea hence the diagnosis of CPV is often a challenge for the veterinarian.
The clinical signs and symptoms of CPV are variable and dependent on age, immunity, co-pathogens (parasites, enteric bacteria, viruses) and infective dose of the virus. These signs can mimic many other diseases that cause vomiting and diarrhea hence the diagnosis of CPV is often a challenge for the veterinarian.
A tentative diagnosis
is often based on the presence of a reduced white blood cell count (leukopenia), clinical signs and
epidemiology. The positive confirmation of CPV infection requires the
demonstration of the virus or virus antigen in the stool 2-4 days after onset of disease by commercial fecal
ELISA tests, or the detection of anti-CPV antibodies in the blood serum.
Occasionally, a dog will have parvovirus but test negative for virus in the
stool. Fortunately, this is an uncommon occurrence. If further confirmation is needed,
stool or blood can be submitted to a veterinary laboratory for additional
tests. The absence of a leukopenia does not mean the dog does not have CPV
infection. Some dogs that become clinically ill may not have a low white blood
cell count.
Treatment
There is no treatment to kill the virus once it infects the dog. However, the virus does not directly cause death; rather, it causes loss of the lining of the intestinal tract, and destroys some blood cell elements. The intestinal damage results in severe dehydration (water loss), electrolyte (sodium and potassium) imbalances, and infection in the bloodstream (septicemia and bacteremia).
There is no treatment to kill the virus once it infects the dog. However, the virus does not directly cause death; rather, it causes loss of the lining of the intestinal tract, and destroys some blood cell elements. The intestinal damage results in severe dehydration (water loss), electrolyte (sodium and potassium) imbalances, and infection in the bloodstream (septicemia and bacteremia).
The first step in
treatment is to correct dehydration and electrolyte imbalances. This requires
the administration of intravenous fluids containing electrolytes. Antibiotics (Cephalosporins, enrofloxicins, or
combinations such as IV ampicillin and gentamicin) and anti-inflammatory drugs
are given to prevent or control septicemia. Antispasmodic drugs are used to inhibit
the diarrhea and vomiting that perpetuate the problems.
Survival Rate
Most dogs with CPV
infection recover if aggressive treatment is used and if therapy is begun
before severe septicemia and dehydration occur. Some breeds, notably the
Rottweiler, Doberman pinscher and English Springer spaniel, have a much higher
fatality rate than other breeds.
Prevention
The best method of protecting your dog against CPV infection is proper vaccination. Puppies receive a Parvo vaccination as part of their multiple-agent vaccine given at 6, 9 and 12 weeks of age. After the initial series of vaccinations, all dogs should be given a booster vaccination at one year. Thereafter your veterinarian will discuss with you an appropriate schedule of revaccination. Dogs in high exposure situations (i.e., kennels, dog shows, field trials, etc.) may be better protected with a booster every six months. Pregnant females might be boostered with a killed Parvo vaccine within two weeks before whelping in order to transfer protective antibodies to the puppies. Your veterinarian should make the final decision about a proper vaccination schedule.
The best method of protecting your dog against CPV infection is proper vaccination. Puppies receive a Parvo vaccination as part of their multiple-agent vaccine given at 6, 9 and 12 weeks of age. After the initial series of vaccinations, all dogs should be given a booster vaccination at one year. Thereafter your veterinarian will discuss with you an appropriate schedule of revaccination. Dogs in high exposure situations (i.e., kennels, dog shows, field trials, etc.) may be better protected with a booster every six months. Pregnant females might be boostered with a killed Parvo vaccine within two weeks before whelping in order to transfer protective antibodies to the puppies. Your veterinarian should make the final decision about a proper vaccination schedule.
Client Education
The stability of the CPV in the environment makes it important to properly disinfect contaminated areas.
This is best accomplished by cleaning food bowls, water bowls, and other contaminated items with a solution of 1/2 cup of chlorine bleach in a gallon of water (133 ml in 4 liters of water). It is important that chlorine bleach be used because most disinfectants, even those claiming to be effective against viruses, will not kill the canine parvovirus.
The stability of the CPV in the environment makes it important to properly disinfect contaminated areas.
This is best accomplished by cleaning food bowls, water bowls, and other contaminated items with a solution of 1/2 cup of chlorine bleach in a gallon of water (133 ml in 4 liters of water). It is important that chlorine bleach be used because most disinfectants, even those claiming to be effective against viruses, will not kill the canine parvovirus.
Dr.
Moses Bwana
Post-grad at the University of Nairobi [Applied
Microbiology]
Department of Veterinary Pathology, Microbiology and Parasitology
Tuesday, 19 January 2016
ZIKA VIRUS DISEASE
ZiKa Virus (ZKV)disease is an emerging mosquito-borne human viral infection that has been ecologically
associated with congenital microcephaly in newborns in Brazil. The general
public is therefore advised to take precautions to reduce the risk of infection
for example: protecting yourself from mosquito bites by wearing long-sleeved
shirts and trousers and keeping doors and windows screened. Pregnant women are advised
to: prevent contact with people traveling from Brazil showing signs of fever/infection,
use pregnancy compatible mosquito repellents and avoid environmental exposures
to chemicals or consumption of teratogenic drugs.
Congenital microcephaly
means the newborn’s head falls below its normal circumference for its gestational
age, sex and race. The small head is the result of a neurodevelopmental disorder
and can be monitored prenatally using ultrasound machines.
The virus (ZKV)
was first isolated in Uganda in 1947 and has since been reported in tropical
areas of western Africa (Nigeria, Sierra Leone, Ivory Coast, Cameroon and Senegal)
and of central Africa (Gabon, Uganda and Central African Republic), in Asia
(Pakistan, Indonesia, Philippines, Malaysia, Cambodia and Thailand) and in
several islands of the pacific region since 2007 (Micronesia, Cook Islands,
French Polynesia, New Caledonia, Guam, Samoa, Vanuatu and Solomon Islands). The
latest (2014) cases of ZKV infection have been reported in the Americas (North-eastern
Brazil in the states of Bahia, Maranhao, Pernambuco, Rio Grande do Norte,
Paraíba and Sergipe). A total of 14835 cases of acute exanthematous illness
have been reported in 12 health districts of Salvador – the third city of Brazil
– between 15 February 2015 and 25 June 2015 with an overall attack rate of 5.5
cases/10 000 inhabitants). The expansion of the ZIKV infections to South
America constitutes a significant development in the epidemiology of this
emerging vector-borne disease.
ZKV dis is caused
by Zika virus (ZIKV), a flavivirus
from the Flaviviridae family and
Spondweni serocomplex. The virus was first identified in 1947 in the Zika forest in Uganda in the rhesus macaque population.
Mosquitoes
remain the main transmitters of the disease with the Aedes mosquitoes (Aedes
aegypti, Aedes hensilii and Aedes
albopictus) being highly implicated.
There is also
evidence that prenatal transmission can occur via the placenta or during the
delivery of a viraemic mother. ZIKV transfusion-derived transmission is theoretically
possible. Possible cases of sexual transmission of ZIKV have been reported but
these three modes of transmission are rare.
The
incubation period of the infection ranges from 3 to 12 days. The disease
symptoms are usually mild and last for 2 to 7days. Infection may go
unrecognized or be misdiagnosed as dengue, chikungunya or other viral
infections giving fever and rash. Asymptomatic infections are common and only
one in four people infected with ZIKV are believed to develop symptoms.
The main
symptoms of ZIKV disease include:
- low-grade fever (<38.5°C)
- transient arthritis/arthralgia with possible joint swelling mainly in the smaller joints of the hands and feet.
- maculo-papular rash often spreading from the face to the body
- conjunctival hyperaemia or bilateral non-purulent conjunctivitis (Red eyes)
- General non-specific symptoms such as myalgia (muscle pains), asthenia and headaches.
Association
with neurological complications is still under investigation ad there has
however been no deaths associated with ZKV infection to date.
Dr.
Moses Bwana
Post-grad
at the University of Nairobi [Applied Microbiology]
Cell: +254729246187; Email: bwanamoses@gmail.com
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