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.

Human and Swine Disease

  

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.

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.

Transmission

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

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])

Department of Veterinary Pathology, Microbiology and Parasitology

Faculty of Veterinary Medicine

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. 

Etiology

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.

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.

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.

Concurrent infection with other gastrointestinal pathogens (Giardia, hookworms and
roundworms, coronavirus) may exacerbate the severity of CPV infection.

Stress of overcrowding, poor nutrition, and age at infection can dictate the outcome of infection.

Transmission

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.

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.

Clinical Signs

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.

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).

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.

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.

Dr. Moses Bwana

Post-grad at the University of Nairobi [Applied Microbiology]

Faculty of Veterinary Medicine

Department of Veterinary Pathology, Microbiology and Parasitology

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.

Epidemiology

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.

Etiology

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.

Transmission

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.

Symptoms

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]

Department of Pathology, Microbiology and Parasitology

Faculty of Veterinary Medicine

Cell: +254729246187; Email: bwanamoses@gmail.com

FOOT-AND-MOUTH DISEASE

                                                                                                                             28th Dec. 2015

Foot and Mouth Disease (FMD) is a highly infectious disease caused by a virus in the genus Aphthovirus, family Picornaviridae. There are seven serotypes of FMD virus (FMDV) namely O, A, C, SAT1, SAT2, SAT3 and Asia1 that affects cloven-hoofed animals and causes disease in important domestic livestock species including; cattle, pigs, Goats and sheep and wild bovids.  In the Greater Horn of Africa region, all the listed strains are present except Asia 1 though serotype C is now less frequent and was last reported in Kenya in the year 2004. Infection with any one serotype does not confer immunity against another and in essence the serotype and their many sub-serotypes are like different FMD diseases in the region. FMD is considered a Transboundary Animal Disease (TAD) with threat to trade of live animals and their products, and is also considered a livestock production disease because of its negative impact on meat and milk production. 

Risk Factors

Close contact of livestock in watering points and in limited pastures during drought periods.

Unregulated trade, livestock movement and proximity between open endemic and closed systems of livestock management

Breed and immunological status: Severity of FMD outbreaks varies with breeds and immunological status of the susceptible population. Improved breeds and exotic breeds show more severe disease compared with local breeds.

Presence of a naive livestock population: Infection of isolated naive populations is usually more severe when compared to endemic populations.

Closed and open management systems: Endemicity is supported by open systems and frequent livestock movements and mixing of different herds as seen in pastoral areas. Closed systems, like in the dairy systems may give rise to epidemic situations of FMD when biosecurity is breached.

Transmission and Spread

Different susceptible species have different epidemiological roles in the maintenance, transmission and spread of FMD. Domestic pigs, wild pigs and warthogs act as amplifier hosts, while the African buffalo can maintain sub-clinical infection with low intermittent viral excretion and act as a reservoir for the SAT viruses. The disease is spread by infected animals through aerosols, contact with contaminated farm equipment, vehicles, clothing or feed, and by domestic and wild predators. Animal movement and wildlife reservoirs are important for transmission of FMD in the region.

Clinical Presentation

FMD should be  suspected in cattle, sheep, goats, pigs and other cloven-hoofed animals if any one or more of the following clinical signs are encountered: Fever (40^oC); unruptured vesicles; blisters and sores in the mouth, tongue, teats and feet at the coronary band and interdigital space; lameness, salivation, discharges from the nose and the mouth.

Diagnosis

Field diagnosis of FMD in cattle, sheep, goats, pigs and other cloven-hoofed animals is based on the main clinical signs which include: Vesicles, blisters and sores in the mouth, interdigital space and coronary band in the feet; Salivation; and Sudden death in young animals. Laboratory diagnosis is based on serological tests (Virus Neutralization, competitive ELISA) and virus isolation, detection and nucleic acid recognition methods (Sandwich ELISA, RT-PCR).

Treatment,Control and Prevention

There is no specific treatment for FMD, but supportive care may be allowed in FMD endemic areas. FMD out- breaks are typically combated through a combined strategy of mass vaccination and animal culling. Livestock movement restriction from outside the ecosystem is important in reducing incursion of new serotypes and sub-serotypes. Ring vaccination within 10 km radius should be applied around outbreak areas starting from clean areas inward during outbreaks. Vaccination should not be done in infected farms.

Containment of FMD will demand considerable efforts in movement restrictions, including quarantine and vaccination. And FMD being endemic throughout the Greater Horn of Africa, regional coordination is essential for its improved control.

Dr. Moses Bwana

Post-grad at the University of Nairobi [Applied Microbiology]

Department of Veterinary Pathology,Microbiology and Parasitology

Faculty of Veterinary Medicine

Cell: +254729246187; Email: bwanamoses@gmail.com