CHAPTER THIRTEEN:
WILDLIFE DISEASES

Dadi-Mamud, Naomi John., Hamzat Aliyu and ALIYU, Danjuma Aliyu

13.1      Introduction

Wildlife refers to animals and other living things including vegetations living in a natural undomesticated habitat. While on the other hand, diseases are conditions in living that is manifested in pathological symptoms not resulting from physical injuries. Thus, wildlife diseases can be described as conditions in wildlife that results in pathological symptoms from the internal working conditions of the body system and not as a result of direct of physical injury

Diseases of wildlife can cause significant illness and death to individual animals and can significantly affects wildlife populations. Wildlife species can also serve as natural hosts of certain diseases that affects human (zoonosis). The diseases agents or parasites that causes these zoonotic diseases can be through the bite of arthropod vectors such as mosquitoes ticks, and mites that have previously fed on an infected animal (World Health Organization, 2021). These zoonotic diseases are primarily diseases acquired within a specific locality, and secondarily, disease of occupation and a vocation. Plague, tularaemia and leiptospirosis have been acquired in the handling and skinning of rodents, rabbits and carnivores. Human have usually acquired disease like Colorado tick fever, Rocky Mountain spotted fever, and Lyme disease because they have spent time in optimal habitats of diseases vectors and hosts.

13.2      DISEASES: THEIR SYMPTOMS, DIAGNOSIS, PREVENTION, AND TREATMENT

Below are some of the diseases that are associated with wildlife, their symptoms, diagnosis, prevention and treatment.

13.2.1  TULAREMIA (RABBIT FEVER)

Tularaemia (also known as rabbit fever or deerfly fever) is an infectious disease of ticks and rabbits that is caused by a bacterium, Francisella tularensis). The disease was first described in Japan in 1837. Its name relates to the description in 1911 of a plague-like illness in the ground squirrels in Tulare County, California (hence the name tularemia) and the subsequent work done by Dr. Edward Francis. Tularaemia occurs throughout North America and in many parts of Europe and Asia. Francisella tularensis is found worldwide in over a hundred species of wild animals, birds and insects. Some examples of animals, other than rabbits, that carry tularemia are meadow mice, ground hogs (woodchucks), ground squirrels, tree squirrels, beavers, coyotes, muskrats, opossums, sheep, and various game birds. There are two common ways through which humans can contract tularaemia from the bite of an infected tick, deerfly (Chrysops discalis), or mosquito: 1) when transmitted to humans by insects; the exposed body surfaces are bitten by the vectors and this results  in pain and fever that is sudden and very severe: 2) when broken skin such as cuts and abrasions comes into direct contact with an infected rabbit carcass (mostly from the rabbit species of the genus Sylvilagus; which are also known as the cottontails)(Center for the Disease Control and Prevention, 2021;Croddy and Krcalova, 2001). Other ways of spreading the disease are drinking contaminated water, inhaling dust from contaminated soil, or handling contaminated pets or paws of animals. However, Human-to-human transmission of tularemia is highly uncommon. 

Symptoms

In humans, tularaemia may appear in two forms depending on how a patient contracted the disease. The most common form is usually acquired through the bite of an infected tick (especially deer ticks and dog ticks) or from contact with infected rabbits. (Note: dog ticks are also called wood ticks and that deer ticks are the primary cause for a very serious disease called Lyme disease) (CDC, 2015; Kwit et al., 2016). Patients will develop an ulcer at the site of infection and lymph glands become inflamed and swollen. Severe fever and flu-like symptoms may accompany the ulcer or lesion. Symptoms start to show within 1-14 days after contracting the disease, with 3-5 days being most common.   The fever generally lasts for 3 to 6 weeks if no type of antibiotic therapy is used to combat the bacteria. Patients with the less common form of tularemia, which occurs mainly after inhalation of bacteria, typically experience sudden chills, fever, weight loss, abdominal pains, tiredness, and headaches. Patients with the above forms and symptoms of tularaemia may develop an unusual pneumonia that can induced fatality.

Symptoms of the disease in a rabbit are a white spotted liver, swollen spleen, and an ulcerated or raw area about ¼ inches in diameter which is where the animal was bitten by a tick or deer fly and thus infected.

 

Transmission

A report of tularaemia outbreaks indicates two primary modes of disease transmission. An increase in the number of reported cases in the eastern and midwestern United States during fall and winter coincides with hunting season when hunters are skinning rabbits (CDC, 2015; Eisen et al., 2008). In the southwestern and western United States, the incidence of tularemia is highest during summer months due to tick bites. The risk of contracting tularemia from rabbits is greatest when handling rabbits after the hunt during the cleaning process. Hunters skinning rabbits are advised to wear protective rubber gloves to reduce the risk of contracting the bacteria that cause tularemia when broken skin comes into contact with an infected carcass or a live, infected rabbit. It is also advised that rabbit meat should be thoroughly cooked before eating. Bacteria that cause tularemia can live for weeks in water, soil, carcasses, and hides, and for years in frozen rabbit meat (Enderlin et al., 2004).

Prevention
Rubber, plastic, or latex gloves should be worn while skinning or handling rabbits, especially if there is an open cuts or abrasions. Wild rabbit and rodent meat should be cooked thoroughly before eating (WHO, 2021). Although this doesn't imply that the meat has to be overcooked that it is not bloody in the middle which is a sign that the meat is still raw or uncooked (Tarnvik, 2007). To avoid the transmission through the bites from the vectors when outdoors, insect repellent apparels that contain DEET (for skin) and/or repellents containing Permethrin (for clothing only) should be used. Tick checks should also be conducted every two to three hours if spending a lot of time outdoors where ticks are in large numbers. If stricken by the ticks, careful removal from the spot is actually recommended immediately with the aid of a tweezers. It is wisely suggested that dead rabbits found in the outdoors are not picked up unnecessarily.

Treatment
Doctors recommend a preventive vaccine for people at high risk of contracting tularemia. Untreated, tularemia (Type B) carries a mortality rate of 5-15%, even higher to about 35% with the typhoidal form (Type A). Appropriate antibiotics lower both mortality rates to about 1%. If there is a suspicion of an infection of tularaemia, adequate professional medical care should be sought immediately. Antibiotics such as streptomycin, gentamicin, and tobramycin have been reported to be effective in the treatment the infectious bacteria (Weber et al., 2012; Dennis et al., 2004; Morner, 1994). Long-term immunity will follow recovery from tularemia. However, reinfection has been occasionally reported in laboratory workers that had not received the Tularemia vaccine (CDC, 2021).

13.2.2  RABIES

Rabies is a zoonotic disease (a disease that is transmitted to humans from animals) that is caused by a virus of the genus Lyssavirus. The disease infects both the domestic and wild animals, and is transmitted to people through close contact with infected saliva via bites or scratches from the animals (WHO, 2023). The distribution of the Rabies is widespread on all continents with the exception of Antarctica; however, more than 95% of human deaths occurred in Asia and Africa. Once symptoms of the disease develop, rabies is nearly always fatal.

Symptoms

The incubation period for rabies is typically 1–3 months, but may vary from <1 week to >1 year. The initial symptoms of rabies are fever and often pain or an unusual or unexplained tingling, pricking or burning sensation (paraesthesia) at the wound site. As the virus spreads through the central nervous system, progressive, fatal inflammation of the brain and spinal cord develops. Two forms of the disease can follow CDC, 2021). People with furious rabies exhibit signs of hyperactivity, excited behaviour, hydrophobia and sometimes aerophobia. After a few days, death occurs by cardio-respiratory arrest. Paralytic rabies accounts for about 30% of the total number of human cases. This form of rabies runs a less dramatic and usually longer course than the furious form. The muscles gradually become paralyzed, starting at the site of the bite or scratch. A coma slowly develops, and eventually death occurs. The paralytic form of rabies is often misdiagnosed, contributing to the underreporting of the disease.

Diagnosis

No tests are available to diagnose rabies infection in humans before the onset of clinical disease, and unless the rabies-specific signs of hydrophobia or aerophobia are present, the clinical diagnosis may be difficult. Post mortem, the standard diagnostic technique is to detect rabies virus antigen in brain tissue by fluorescent antibody test (Pearson, 1998). Currently, the diagnosis is usually done through testing the saliva, spinal fluid and skin samples.

 

Transmission

People are infected through the skin following a bite or scratch by an infected animal. Dogs are the main host and transmitter of rabies. They are the source of infection in all of the estimated 55 000 human rabies deaths annually in Asia and Africa. Bats are the source of most human rabies deaths in the United States of America and Canada. Bat rabies has also recently emerged as a public health threat in Australia, Latin America and Western Europe. Human deaths following exposure to foxes, raccoons, skunks, jackals, mongooses and other wild carnivore host species are very rare. Transmission can also occur when infectious material – usually saliva – comes into direct contact with human mucosa or fresh skin wounds. Human-to-human transmission by bite is theoretically possible but has never been confirmed (Rappini et al., 2007). Rarely, rabies may be contracted by inhalation of virus-containing aerosol or via transplantation of an infected organ. Ingestion of raw meat or other tissues from animals infected with rabies is not a source of human infection.

Treatment after Exposure

Effective treatment soon (within a few days, but as soon as possible) after exposure to rabies can prevent the onset of symptoms and death. Post-exposure prevention consists of local treatment of the wound, administration of rabies immunoglobulin and immediate vaccination.

Local Treatment of the Wound

Removing the rabies virus at the site of the infection by chemical or physical means is an effective means of protection. Therefore, prompt local treatment of all bite wounds and scratches that may be contaminated with rabies virus is important. Recommended first-aid procedures include immediate and thorough flushing and washing of the wound for a minimum of 15 minutes with soap and water, detergent, povidone iodine or other substances that kill the rabies virus. The recommended post-exposure prophylaxis depends on the type of contact with the suspected rabid animal (Ryan and Ray, 2004).

13.2.3 PLAGUE (Yersinia pestis Infection)

Plague, caused by a bacterium called Yersinia pestis mostly found in small mammals and their fleas.  It is characterised by the periodic disease outbreaks in rodent populations, some of which have a high death rate. Once there is an outbreak, hungry infected fleas that have lost their normal hosts seek other sources of blood, thus increasing the increased risk to humans and other animals frequenting the area (Trevisanato, 2007). Epidemics of plague in humans usually involve house rats and their fleas with an epidemic that continue to occur in some developing countries with more rural areas. Many other rodent species, for instance, prairie dogs, wood rats, chipmunks, and other ground squirrels and their fleas, suffer plague outbreaks and some of these occasionally serve as sources of human infection. Deer mice and voles are thought to maintain the disease in animal populations but are less important as sources of human infection. Other less frequent sources of infection include wild rabbits, and wild carnivores that pick up their infections from wild rodent outbreaks. Domestic cats (and sometimes dogs) are readily infected by fleas or from eating infected wild rodents. Cats may serve as a source of infection to persons exposed to them. Pets may also bring plague-infected fleas into the home. Between outbreaks, the plague bacterium is believed to circulate within populations of certain species of rodents without causing excessive mortality (Office International des Épizooties, 2000). Such groups of infected animals serve as silent, long-term reservoirs of infection.

Distribution

In the United States during the 1980s, plague cases averaged about 18 per year. Most of the cases occurred in persons under 20 years of age. About 1 in 7 persons with plague died. Worldwide, there are 1,000 to 2,000 cases each year. During the 1980s epidemic plague occurred each year in Africa, Asia, or South America. Epidemic plague is generally associated with domestic rats (CDC, 2021). Almost all of the cases reported during the decade were rural and occurred among people living in small towns and villages or agricultural areas rather than in larger, more developed, towns and cities.

Transmission

Plague is transmitted from animal to animal and from animal to human by the bites of infective fleas. Less frequently, the organism enters through a break in the skin by direct contact with tissue or body fluids of a plague-infected animal, for instance, in the process of skinning a rabbit or other animal (kwit et al., 2019). Plague is also transmitted by inhaling infected droplets expelled by coughing, by a person or animal, especially domestic cats, with pneumonic plague. Transmission of plague from person to person is uncommon but does occur as an important factor in plague epidemics in some developing countries.


 

Diagnosis

The pathogenomic sign of plague is a very painful, usually swollen, and often hot-to-the touch lymph node, called a bubo. This is usually accompanied with fever, extreme exhaustion. A history of possible exposure to rodents, rodent fleas, wild rabbits, or sick or dead carnivores should serve as a signal of potential plague infection. Onset of bubonic plague is usually 2 to 6 days after a person is exposed (CDC, 2021; Nelson et al., 2021). Initial manifestations include fever, headache, and general illness, followed by the development of painful, swollen regional lymph nodes. Occasionally, buboes cannot be detected for a day or so after the onset of other symptoms. The disease progresses rapidly and the bacteria can invade the bloodstream, producing severe illness, called plague septicemia.

Once a human is infected, a progressive and potentially fatal illness generally begins unless specific antibiotic therapy is given. Progression leads to blood infection and, finally, to lung infection. The infection of the lung is termed plague pneumonia, and it can be transmitted to others through the expulsion of infective respiratory droplets by coughing (CDC, 2021; Nelson et al., 2021). The incubation period of primary pneumonic plague is 1 to 3 days and is characterized by development of an overwhelming pneumonia with high fever, cough, bloody sputum, and chills. For plague pneumonia patients, the death rate is over 50%.

Prevention

Plague will probably continue to exist in its many localized geographic areas around the world, and plague outbreaks in wild rodent hosts will continue to occur. Attempts to eliminate wild rodent plague are costly and futile. Therefore, primary preventive measures are directed toward reducing the threat of infection in humans in high-risk areas through three techniques - environmental management, public health education, and preventive drug therapy.

Antibiotics may be taken in the event of exposure to the bites of wild rodent fleas during an outbreak or to the tissues or fluids of a plague-infected animal. Preventive therapy is also recommended in the event of close exposure to another person or to a pet animal with suspected plague pneumonia. For preventive drug therapy, the preferred antibiotics are the tetracyclines, chloramphenicol, or one of the effective sulphonamides (CDC, 2021; Nelson et al., 2021).


 

Treatment

As soon as a diagnosis of suspected plague is made, the patient is isolated, and local and state health departments notified. Confirmatory laboratory work should be initiated, including blood cultures and examination of lymph node specimens if possible. Drug therapy should begin as soon as possible after the laboratory specimens are taken. The drugs of choice are streptomycin or gentamycin, but a number of other antibiotics are also effective (OIE, 2000). Those individuals closely associated with the patient, particularly in cases with pneumonia, should be traced, identified, and evaluated. Contacts of pneumonic plague patients should be placed under observation or given preventive antibiotic therapy, depending on the degree and timing of contact

Epidemic plague is best prevented by controlling rat populations in both urban and rural areas. This goal has been reached in the cities, towns, and villages of most developed countries (James and Berger, 2006). It has not been achieved in either the rural or urban areas of many developing countries where the threat of epidemic plague continues to exist. Control of plague in such situations requires two things: 1) close surveillance for human plague cases, and for plague in rodents, and 2) the use of an effective insecticide to control rodent fleas when human plague cases and rodent outbreaks occur.

13.2.4    MYCOBACTERIUM TUBERCULOSIS INFECTION

 Tuberculosis is one of the oldest of the recognized diseases in humans and animals.  It is caused by a species of pathogenic bacteria of family Mycobacteriaceae. It was not until 1882, that the cause of the disease became known. Dr. Robert Koch, the noted German scientist, proved that a microorganism could be isolated from the characteristic tubercules that form during the typical TB disease process. The rod-shaped organism as seen under the microscope varies in size, from about 1 to 4 microns (about 6,000-16,000 laid end to end equals 1 inch). Koch showed that these same “rods” can cause the typical tuberculosis disease when inoculated into another animal.  Although it was originally called Koch’s bacillus, the organism was later given the scientific name of Mycobacterium tuberculosis as it is still known today.

The disease may be contracted in a variety of ways and affects many organs of the body (Todar, 2016). Most of the time, the bacilli are inhaled via infected droplets from an infected person’s or animal’s lungs, or by ingesting contaminated food, milk or water. Once the bacilli get into a susceptible organism, a number of events occur which cause the characteristic disease.  It generally starts in the areas where the exposure occurs.  The lungs are often attacked, but other parts of the body can be affected. When it gets into the lymph system, it can travel to all parts of the body.  Wherever the bacilli lodge, invader-fighting white blood cells are attracted to the bacilli invaders and attempt to ingest them.  The bacillus has a waxy coating that is very resistant to the white cells attempts to digest it.  The invader fighting cells then attempt to isolate bacilli inside a hard nodule and a “tubercle” is thus formed (CDC, 2015).  If the wall of the tubercle is dense and effective in encapsulating all the mycobacterium bacteria, there will be little advancement of the disease and the tubercule may even calcify.  But, if the bacilli are not completely contained, a spreading lesion will ensue.  Bacilli may escape from the lesion and move to other parts of the body.  Wherever invader cells lodge, the disease process starts over again.  During the process of the disease development and expansion, the animals become emaciated, lethargic, organs become damaged and the animal weakens and dies.  

Diagnosis

Tuberculosis lesions cannot always be seen or palpated, so clinical signs are not reliable for a diagnosis.  The intradermal tuberculin test is still the most important diagnostic test for TB.  Radiography is useful for imaging lesions in non-human primates and small animals. Discharges and sputum can be examined microscopically, but diagnosis other than the tuberculin test requires culturing tissue samples on selective media which can take 4-8 weeks (Ryan and Ray, 2004).  The intradermal test made from mycobacterial antigen is the one most used for large animals. A positive reaction includes skin swelling. The test is not perfect as there are cross reactions with other strains of mycobacteria and false negatives may occur under certain conditions.  Current research efforts are trying to find improved diagnostic methods. An interferon-based assay has recently been developed and has proven beneficial. Other tests are also being evaluated.

Control Measures.

The trend toward intensive agriculture has made control more difficult. Also, the presence of wild animals as reservoirs of the Mycobacterium (e.g. badgers in the UK, brush-tail possums in New Zealand, and white-tailed deer in the US) make it very difficult to eradicate the disease.  Generally, there are three approaches currently used to the control the disease in domestic animals: 1) test for TB with the intradermal tuberculin test and either slaughter, 2) segregate or 3) treat with drugs (CDC, 2018).  The removal of reacting presumed infected animals is the only assured approach to eradicating the disease. This is however limited where pastured animals are infected by exposure to diseased wild animals.   The use of drugs is discouraged due to exposure of humans to animals being treated, possible development of drug resistant strains, and the expense to producers. The efficacy of a live vaccine made from the attenuated strain of Mycobacterium tuberculosis BCG (Bacilli Calmette-Guerin) has proven variable and use of this vaccine may confound interpretation of current diagnostic tests. Improved vaccines are currently being evaluated in research trials.

13.2.5  Lymphocytic Choriomeningitis (LCM)

Lymphocytic choriomeningitis (LCM), is a rodent-borne viral infectious disease that presents as aseptic meningitisencephalitis or meningoencephalitis. Its causative agent is the Lymphocytic Choriomeningitis Virus (LCMV), a member of the family Arenaviridae. The name was coined by Charles Armstrong in 1934. In the Gale Encyclopedia of Medicine, second edition, lymphocytic choriomeningitis (LCM) is defined as “a viral infection of the membranes surrounding the brain and spinal cord and of the cerebrospinal fluid. The name is based on the tendency of an individual to have abnormally high levels of lymphocytes during infection. Choriomeningitis is cerebral meningitis in which there is marked cellular infiltration of the meninges, often with a lymphocytic infiltration of the choroid plexuses (Albarino et al., 2007).  LCMV is an enveloped virus with a helical nucleocapsid containing an RNA genome consisting of two single-stranded RNA segments. The L strand is ambisense RNA and encodes the polymerase and z protein while the S strand is ambisense and encodes the nucleo-protein and glycoproteins. The first arenavirus, lymphocytic choriomeningitis virus (LCMV), was isolated in 1933 by Charles Armstrong during a study of an epidemic in St. Louis. Although not the cause of the outbreak, LCMV was found to be a cause of nonbacterial or aseptic meningitis. LCMV is naturally spread by the common house mouseMus musculus.  Once infected, these mice can become chronically infected by maintaining virus in their blood and/or persistently shedding virus in their urine. 

Infection

Infected female mice are reported to usually transmit infection to their offspring (vertical transmission), which in turn become chronically infected. Other modes of mouse-to-mouse transmission include nasal secretions, milk from infected dams, bites, and during social grooming within mouse communities. Airborne transmission also occurs.  The virus seems to be relatively resistant to drying and therefore humans can become infected by inhaling infectious aerosolized particles of rodent urine, faeces, or saliva, by ingesting food contaminated with virus, by contamination of mucus membranes with infected body fluids. Direct exposure to cuts, abrasions or other open wounds to virus-infected blood is another way of acquiring this infection. The only documented cases of transmission from animals have occurred between humans and mice or hamsters (Jahrling and Peters, 1992). Cases of lymphocytic choriomeningitis have been reported in North and South America, Europe, Australia, and Japan, particularly during the 1900s. However, infection may occur wherever an infected rodent host population exists. 

Symptoms

LCMV infection manifests itself in a wide range of clinical symptoms, and may even be asymptomatic for immunocompetent individuals. Onset typically occurs between one or two weeks after exposure to the virus and is followed by a biphasic febrile illness. During the initial or prodromal phase, which may last up to a week, common symptomatic features include fever, lack of appetite, headache, muscle aches, malaise, nausea, and/or vomiting. Less frequent symptoms include a sore throat and cough, as well as joint, chest, and parotid pain (CDC, 2005). The onset of the second phase occurs several days after recovery, and consists of symptoms of meningitis or encephalitis. Pathological findings during the first stage consist of leukopenia and thrombocytopenia. During the second phase, typical findings include elevated protein levels, increased leukocyte count, or a decrease in glucose levels of the cerebrospinal fluid).

Diagnosis

Current or previous infection can be detected through a blood test. However, some authors note that such complement-fixation tests are insensitive and should not be used for diagnosis. Timeliness of diagnosis is important not only in expediting treatment of infected persons, but also in preventing further LCM transmission to other workers and animals (CDC, 2005). Clinical diagnosis of LCM can be made by the history of prodrome symptoms and by considering the period of time before the onset of meningitis symptoms, typically 15–21 days for LCM.

Pathological diagnosis of congenital infection is performed using either an immunofluorescent antibody (IFA) test or an enzyme immunoassay to detect specific antibody in blood or cerebrospinal fluid. Diagnoses are subject to methodological shortcomings in regard to specificity and sensitivity of assays used. For this reason, LCMV may be more common than is realized.

Treatment

Currently, there is no LCMV - specific treatment for humans; although nucleoside analog ribavirin is used in some cases due to the inhibitory effect the agent has in vitro on arena viruses. However, there is not sufficient evidence for efficacy in humans to support routine use. Early and intravenous ribavirin treatment is required for maximal efficacy, and it can produce considerable side effects (CDC, 2005). Use of ribavirin during pregnancy is generally not recommended, as some studies indicate the possibility of teratogenic effects. If aseptic meningitis, encephalitis, or meningoencephalitis develops in consequence to LCMV, hospitalization and supportive treatment may be required. In some circumstances, anti-inflammatory drugs may also be considered. In general, mortality is less than one percent.

13.2.6 HISTOPLASMOSIS INFECTION

Histoplasmosis is a fungal infection that can infect cats, dogs, and people. It is caused by Histoplasma capsulatum, which is found in the soil that contains most of the droppings from the afore-mentioned animals.  It enters the body through the lungs. The disease causes a variety of respiratory and intestinal symptoms. Other symptoms include; fever, cough fatigue and body aches. Histoplasma is predominantly isolated in areas that are moist and humid and grows best in soils that contain nitrogen-rich organic matter such as bird or bat droppings. Cats and dogs can both be infected (Assi et al., 2007). Infections are more common in outside cats and dogs, particularly in hunting dogs. Animals of any age can get histoplasmosis. However, most infections occur in animals under four years of age.

Transmission

Cats get infected by inhaling the spore-like particles of the fungus that inhabit the soil. These tiny particles are small enough to reach the lower respiratory tract (lungs). A few cases of infection in strictly indoor animals have been reported and it is suspected that potting soil or dirt brought in from outside may be the source of infection in these animals (CDC, 2020).


 

Symptoms

The symptoms are varied and depend somewhat on the severity of the infection. Histoplasmosis infections start in the lung. As the fungal organisms replicate, the animal can develop a respiratory form of the disease. Many healthy animals will recover from the milder respiratory infections on their own. In other animals, particularly ones with a poor or deficient immune system, the respiratory infection may become more severe or the infection may spread to the gastrointestinal (GI) system, lymph nodes, spleen, liver, or eyes. The most common symptoms in the cat or dog are weight loss, fever, loss of appetite, and depression. Laboured breathing with increased lung sounds is present, and many animals may also have a cough (Assi et al., 2007). In addition to these symptoms, both cats and dogs may be anaemic and have pale gums.

Diagnosis

Diagnosis of histoplasmosis is often made from information obtained from the history, symptoms, x-rays of the chest and abdomen, and by finding the organisms in the infected tissue (Assi et al., 2007). A needle aspirate or biopsy of the infected tissue can often yield some of the small budding fungal organisms.

Prevention

There is no vaccine to protect against histoplasmosis. The best prevention is to avoid areas where histoplasmosis is known to be a problem. Areas where large numbers of birds or bats roost should also be avoided. Infections are not transmitted between infected animals or between animals or humans. While humans can get the infection, they get it from the fungal spores in the soil just like animals do.

Treatment

In many simple cases of the respiratory form of histoplasmosis, treatment may not be necessary because the animal will clear the infection on its own. But because of the risk of the infection spreading or becoming more severe, treatment is often initiated as soon as a positive diagnosis is made. The treatment of choice is an oral antifungal drug. The most commonly used ones are itraconazole or fluconazole. Ketoconazole is sometimes used when cost is a consideration, though it may not be as effective and can be more toxic than itraconazole. The treatment usually lasts several months or longer. The success in treating histoplasmosis is very good if the correct treatment is used and instituted before the animal becomes too debilitated (CDC, 2020).

13.2.7 GIARDIASIS

Giardiasis is an intestinal infection caused by a parasitic protozoan (single celled organism) called Giardia lamblia. These germs are found mostly on surfaces, in soil, food or water that has been contaminated with faeces from infected animals.  These protozoans are found in the intestines of many animals, including dogs and humans. This microscopic parasite clings to the surface of the intestine, or floats free in the mucous lining the intestine (Beer et al., 2017; Nakao et al., 2017). Giardia occurs in two forms: a motile feeding stage that lives in the intestine, and a non-motile cyst stage that passes in the faeces. The giardia trophozoite - which is the active stage of the organism - inhabits the small intestine of the dog. The trophozoite stage is tear-drop shaped, binucleated, and has four pairs of flagella. It attaches to the cells of the intestine with its adhesive disc and rapidly divides to produce a whole population of trophozoites. As they detach, they may be swept down the intestine. If intestinal flow is fast then they may appear in the faeces. However, if they have time, encystment occurs as the parasite travels to the large intestine (CDC, 2020). The cyst is fairly resistant, and can survive for several months outside of a host's body as long as sufficient moisture is provided. The cyst is oblong in shape with four nuclei that are sometimes distinctly visible. Mature cysts are usually found in the faeces of infected animals. Other animals become infected by ingesting the cysts that passed from the body in faeces. These ingested cysts then break open inside the small intestine to release the motile feeding stage (trophozoite). Giardia increases their numbers by each organism dividing in half which is called binary fission.   

Transmission
Giardia lives and reproduces in the small intestine of host animals.  Giardia trophozoites, the free-living stage of the organism, form infective cysts that are passed out in the faeces (Beer et al., 2017; Nakao et al., 2017).  If the cysts are present in a wet or damp environment they can survive in a viable state for a few weeks to several months.  Giardia infections are transmitted via ingestion of trophozoites or cysts in contaminated water or food. If a giardia cyst is ingested, the cyst wall is broken down during the digestive process and the trophozoite stage begins to colonize the upper small intestine. Transmission also occurs by direct contact, especially with asymptomatic carriers. More recently, giardiasis has also been recognized as being able to be sexually transmitted. Giardia is so prevalent throughout North America because it is highly contagious. The ingestion of as few as one or more giardia cysts may cause the disease, as contrasted to most bacterial illnesses where hundreds to thousands of organisms must be consumed to produce illness (Beer et al., 2017; Nakao et al., 2017). Giardia causes its unpleasant effects on the body not by invading the tissues, but simply by being in the way. It multiplies to the point where it sorts of paves the lining of the intestine and blocks normal digestion (malabsorption). This causes only partially digested food to get lower in the digestive tract than it should, causing diarrhea.

Symptoms

The trophozoites divide to produce a large population, and then they begin to interfere with the absorption of food. Clinical signs range from none in asymptomatic carriers, to mild recurring diarrhea consisting of soft, light-coloured stools, to acute explosive diarrhea in severe cases. Other signs associated with giardiasis are weight loss, listlessness, fatigue, mucus in the stool, and anorexia (Beer et al., 2017). These signs are also associated with other diseases of the intestinal tract, and are not specific to giardiasis. These signs, together with the beginning of cyst shedding, begin about one-week post-infection. There may be additional signs of large intestinal irritation, such as straining and even small amounts of blood in the faeces (CDC, 2021; Beer et al., 2017). Usually, the blood picture of affected animals is normal, though occasionally there is a slight increase in the number of white blood cells and mild anaemia. Without treatment, the condition may continue, either chronically or intermittently, for weeks or months.

Diagnosis

Diagnosing giardia is not easy. Diagnosis can be done in one of two ways: via faecal sample by a Vet or via educated evaluation of clinical findings by the breeder/owner or the Vet. Faecal sample analysis is not straightforward. Even when a flare is at its worst, the cysts will not be shedding in every single stool. Therefore, a negative report does not rule out giardia. The most thorough way to assess is to collect a sample from every single stool produced for 48 to 72 hours and have a Vet examine it using the giardia test kit. The giardia test is a monoclonal antibody-based ELISA for the rapid detection of Giardia lamblia cysts antigen in stool specimens and serves as an in vitro aid in the diagnosis of giardiasis (Beer et al., 2017).


 

Treatment

Infection may be treated using one of a number of different drugs that are available through Vet Supply Stores. The treatment of choice is often with Metronidazole (brand name Flagyl). Metronidazole kills off the giardia and reduces the numbers to the level the dog's immune system can handle. Adaptations that may be made to try to improve the success rate of a treatment regime include extending the duration and dose of the treatment. Care must obviously be taken with this approach to make sure that an adequate safety margin is always maintained (Beer et al., 2017). Another approach is to retreat after an interval of one week. Alternatively, repeat faecal samples may be collected one week after the treatment and dogs which are still passing cysts can be identified and treated. It should be recognized that, when treating a large number of dogs, whichever of these treatment strategies is adopted, there may be one or two dogs that remain as carriers of infection that will act as a potential source for reintroducing the infection into your entire kennel.

Prevention

 It is very difficult to prevent the entry of an infection that is known to be carried by a percentage of normal dogs into a kennel. However, an initial period of isolation for all new entrants into kennels, for perhaps ten days, would reduce the risk of an infected dog spreading a large number of cysts around the main kennel area (CDC, 2021). All dogs could be observed and any infection present, which in the case of giardia might be exacerbated by the stress of entry in kennels, could be identified and treated before entry into the main kennels, Dogs should be prevented from access to foul water that may contain large numbers of cysts (e.g: river-flooded paddocks). Small numbers of cysts may occasionally be present in the potable water supply but the risk of this being a major source of infection is small (CDC, 2021). It is best to use chlorinated water for the dog’s drinking water as much as possible. When using non-chlorinated water from a well, lake, or stream, there is need to chlorinate the water. To chlorinate drinking water: Use only liquid bleach that contains 5.25% sodium hypochlorite as its only active ingredient and avoid soap. Use a scant 4 drops of Clorox bleach per quart of water or 2 teaspoons per 10 gallons. As an alternate method of purification, you can also boil all of your dog's drinking water. To make sure the water is completely free from living bacteria and protozoans, there is need to bring the water to a rapid boil for a minimum of five (5) minutes. However, cool moist conditions favour the survival of the organism; therefore, simply by keeping everything clean, disinfected, and dry there will be a lot of extermination of these parasites (Daily et al., 2010).

13.2.8 HANTAVIRUS PULMONARY SYNDROME (HPS)

Hantavirus (Sin Nombre virus) belongs to the bunyaviridae family of viruses that is mostly found in the Wild rodents (cotton and rice rats, the white-footed mouse), but particularly deer mice (Peromyscus spp). The disease is recognised as one of the severe respiratory and occasionally fatal infection of human. The main source of the disease is the infestation of the wild rodents that shed the virus through urine, droppings, and saliva (Vaheri et al., 2008; Evander et al., 2007) HPS is majorly transmitted to humans through a process called aerosolization.  Humans become infected by breathing in these infectious aerosols.

Symptoms

In the carrier organisms, they are usually asymptomatic with no outward visible signs of illness, however in human, there are flu-like symptoms such as fever, chill, muscle ache and headache. There is possible likelihood of a respiratory failure which may lead to death. A case of renal syndrome has also been reported in some humans (CDC, 2021).

Treatment

Since diagnosing this infection is difficult, however, when there are symptoms of a typical influenza, the test can also be carried out for it. Although there is no accepted drug for the treatment of the virus, however, practicing a good personal hygiene such as washing of hands after handling animals or nest materials. Since Hantavirus can persist for a few days in the environments. It is recommended that wearing of gloves and facemasks when working with rodents or in potentially contaminated areas should be practised. In case of a development of fever or respiratory illness in any of the handlers of the wild rodents, medical attention should be sought immediately (Heyman and Vaheri, 2008).

13.2.9 BRUCELLOSIS

Brucellosis is a zoonotic disease that is highly contagious. The illness is also known as Bang's disease, Crimean fever, Gibraltar fever, Malta fever, Maltese fever, Mediterranean fever, Rock fever, or undulant fever. It is caused by the ingestion of unsterilized milk or meat from infected animals or close contact with their secretions (OIE, 2000). The transmission of the disease from human to human is through sexual contact or from mother to child which although is rare but possible. The causative bacteria, Brucella spp. are small, gram-negative, non-motile, Non-spore-forming and rod shaped (coccobacilli). They function as facultative intracellular parasites causing chronic disease, which usually persists for life. Symptoms include profuse sweating and joint and muscle pain. Brucellosis has been recognized in animals including humans since the 20th century. Species infecting domestic livestock are B. melitensis (goats and sheep), B. suis (pigs), B. abortus (cattle and bison), B. ovis (sheep), B. canis (dogs). B. abortus also infects bison and elk in North America. Brucella species have also been isolated from several marine mammal species (pinnipeds and cetaceans). The bacterium, Brucella abortus is the principal cause of brucellosis in cattle. The bacteria are shed from an infected animal at or around the time of calving or abortion. Once exposed, the likelihood of an animal becoming infected is variable, depending on age, pregnancy status, and other intrinsic factors of the animal, as well as the number of bacteria to which the animal was exposed (Pearson, 1998). The disease has been classified as an occupational hazard for people who worked in the livestock sector. The most common clinical signs of cattle infected with Brucella abortus are high incidences of abortions, arthritic joints and retained after-birth. There are two main causes for spontaneous abortion in animals.

The causative agent of brucellosis in dogs is Brucella canis. It is transmitted to other dogs through breeding and contact with aborted foetuses. Brucellosis can occur in humans that come in contact with infected aborted tissue or semen. The bacteria in dogs normally infect the genitals and lymphatic system, but can also spread to the eyekidney, and intervertebral disc (causing discospondylitis). Symptoms of brucellosis in dogs include abortion in female dogs and scrotal inflammation and orchitis (inflammation of the testicles) in males. Fever is uncommon. Infection of the eye can cause uveitis, and infection of the intervertebral disc can cause pain or weakness. Blood testing of the dogs prior to breeding can prevent the spread of this disease. It is treated with antibiotics, as with humans, but it is difficult to cure (WHO, 2021)

Symptoms

Brucellosis in humans although very rare is associated with the consumption of unpasteurized milk and soft cheeses made from the milk of infected animals, primarily goats, infected with Brucella melitensis and with occupational exposure of laboratory workers, veterinarians and slaughterhouse workers. Some vaccines used in livestock, most notably B. abortus strain 19, also cause disease in humans if accidentally injected (CDC, 2021). Brucellosis induces inconstant fevers, sweating, weakness, anaemiaheadachesdepression and muscular and bodily pain.

The symptoms are like those associated with many other febrile diseases, but with emphasis on muscular pain and sweating. Flu-like symptoms are also very common for the infection.  The duration of the disease can vary from a few weeks to many months or even years. In the first stage of the disease, septicaemia occurs and leads to the classic triad of undulant fevers, sweating (often with characteristic smell, likened to wet hay) and migratory arthralgia and myalgia. If untreated, the disease can give origin to focalizations or become chronic. The focalizations of brucellosis occur usually in bones and joints and spondylodiscitis of lumbar spine accompanied by sacroiliitis is very characteristic of this disease. Orchitis is also frequent in men.

Treatment

Antibiotics like tetracyclinesrifampicin,andthe aminoglycosides streptomycin and gentamicin areeffective against Brucella bacteria. However, the use of more than one antibiotic is needed for several weeks, because the bacteria incubate within cells. However, it should be noted that the main way of preventing brucellosis is by using fastidious hygiene in producing raw milk products, or by pasteurizing all milk that is to be ingested by human beings, either in its unaltered form or as a derivate, such as cheese (Ryan and Ray, 2004).

13.2.10      EBOLA VIRUS DISEASE

Ebola Virus Disease previously called Ebola haemorrhagic fever is severe and fatal in human. Although it is a very rare disease, the virus is transmitted to human from wild animals and quickly spread among the population through its human-to-human transmission (WHO, 2021; CDC, 2021). It causes acute and serious illness that easily kill an infected person if left untreated. It first appeared in Congo near River Ebola from where it got its name. However, the outbreak is presently restricted to Africa with the West Africa been the most hit. An index case of Ebola was reported in Nigeria on 20th July, 2014 from a Liberia-American named Patrick Sawyer. All in all, 20 cases were reported with 8 deaths. The Ebola virus belongs to Filoviridae which includes other two genera.


 

Transmission

Fruit bats of the family Pteropodidae were first believed to the natural host of the Ebola virus. The transmission of the virus is through human contact with the animal secretions such as blood, organs or other body fluid of the carrier organisms. This further spread to human through the direct contact with an infected person secretion (WHO, 2021; CDC, 2021).

Symptoms

The virus has an incubation period of between 2 to 21 days with manifesting symptoms that include sudden debilitating fever, muscle pain, headache and sore throat. These are subsequently followed by vomiting, diarrhea, skin rash, impaired kidney and liver function. In some severe cases, internal and external bleeding occurred.

Diagnosis

It is difficult to distinguish Ebola virus disease from some infectious diseases but through certain medical approaches such as antigen detection test, virus culture isolation, reverse transcription polymerase, the virus can be detected (WHO, 2021; CDC, 2021).

Treatment  

Isolation and early incubation of infected patient is a way of managing the disease. Frequent rehydration and treatment of disease-specific symptoms is another method of improving the infect person survival. Presently, there are no vaccines to cure the virus, however, trial vaccines are been tested for safety purpose (CDC, 2021; WHO, 2021).

13.2.11      TOXOCARIASIS

 This is a parasitic disease that is caused by the infection of a type of roundworm found in dogs or cats.  The disease can result in a serious illness eye, and organ damages. This disease affect children, dog or cat owners and those that have affection for dirt (CDC, 2021). The infection occurs when people accidentally swallow dirt that has been contaminated with dog faeces containing Toxocara eggs. Though very rare, infection can also be gotten through the consumption of undercooked meat containing Toxocara larvae. However, it is not spread like cold or flu that is transmitted by person-person contact.


 

Symptoms

Majority of those infected with Toxocariasis especially Adults doesn’t exhibit symptoms and get sick, however, children may fall sick and show symptoms such as organ damage, breathing issue, stomach pain, vision problems.

Prevention

The prevention of toxocariasis simply entails adopting hygienic practices especially around the dogs and cats. The practice may include teaching children the importance of washing hands after playing with dirt. Sandboxes should be covered and animals should be restricted to their confines. Dog and cat wastes should be disposed off appropriately. And finally, regular check-up of pets to avoid infection with Toxocara should be adopted (CDC, 2021).

References

Albarino, C.G., Palacios, G., Khristova, M.L. (2010). High Diversity and Ancient common Ancestry of Lymphocytic Choriomeningitis Virus. Emerging Infectious Diseases. 16(7):1093-1100.

Assi, M.A., Sandid, M.S., Baddour, L.M., Robert, G. D. and Walker, R.C. (2007). Systemic Histoplasmosis: A 15 years Retrospective Institutional Review. Medicine, 86(3):162-169.

Beer, K.D., Collier, S.A., Du, F., Gargano, J.W. (2017). Giardiasis Diagnosis and Treatment practices among Commercially Insured Persons in United State. Clinical infectious Diseases,64(4):1244-50

CDC (2020). Diseases Fact Check via www.cdc.gov/fact-sheets/details/disease of wildlife. Retrieved on 21st December, 2021.

CDC (2021). Diseases Fact Check via www.cdc.gov/fact-sheets/details/disease. Retrieved on 21st June, 2021.

CDC, (2015). Notes from the Field: Increase in Human Cases of Tularemia — Colorado, Nebraska, South Dakota, and Wyoming, January–September 2015.

Centers for Disease Control. Update: Interim Guidance for Minimizing Risk for Human Lymphocytic Choriomeningitis Virus Infection Associated with Pet Rodents. Morbidity Mortality Weekly Report. 2005;54(32):799-801.

Croddy, E. and Krcalova, S. (2001). Tularemia: Biological Warfare, and the Battle for Stalingrad (1942-1943). Military Medicine, 166 (10):356-764.

Daily, E.R., Ray, S.J., and Blaney, D.D. (2010). Outbreak of Giardiasis associated with Community Drinking Water Source. Epidemiological Infection,138(4):491-500

Dennis, D.T., Inglesby, T.V. and Henderson, D.A.  (2001). Tularaemia as a Biological Weapon: Medical and Health Management. JAMA, 285(21):2763-273.

Eisen, R.J., Mead, P.S., Meyer, A.M., Pfaff, L.E., Bradley, K.K., and Eisen, L. (2008). Ecoepidemiology of Tularemia in the southcentral United States. American Journal of Tropical Medical Hygiene,78(4):586-94.

Enderlin, G., Morales, L., Jacobs, R.F. and Cross, J.T. (1994). Streptomycin and Alternative Agents for the Treatment of Tularaemia: Review of the Literature. Clinical Infectious Diseases, 19 (1)42-47.

Evander, M., Eriksson, I., Pettersson, L., Juto, P., Ahlm, C.,  and Olsson, G.E. (2007). Puumala Hantavirus Viremia Diagnosed by Real-time Reverse Transcriptase PCR using Samples from Patients with Hemorrhagic Fever and Renal Syndrome. Journal of Clinical Microbiology, 45:2491–97.

Fact Sheets | Infection Control & Prevention | Fact Sheet – BCG Vaccine | TB | CDC". www.cdc.gov. 11 December 2018. Retrieved 12 November 2021.

Fitzgerald, D.W., Sterline, T.R., and Haas, D.W. (2015). 251 – Mycobacterium tuberculosis". In Bennett JE, Dolin R, Blaser MJ (eds.). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Elsevier Saunders. p. 2787. 

 George, W. B. and James, H. S. (1994). Handbook of Zoonoses: Bacterial, Rickettsia, Chlamydial and Mycotic. CRC Press: 117

Heyman, P., and Vaheri, A. (2008). Situation of Hantavirus Infections and Haemorrhagic Fever with Renal Syndrome in European Countries as of December 2006. Eurosurveillance, 18(28):1–8.

Jahrling, P.B., and Peters, C.J. Lymphocytic Choriomeningitis Virus. A Neglected Pathogen of Man. Archives of Pathology & Laboratory Medicine. 1992;116(5):486-8.

James, W.D and Berger, T. G. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. 

Kwit, N.A., Schwartz, A., Kugeler, K.J., Mead, P.S., Nelson, C.A. (2019). Human Tularaemia associated with Exposure to Domestic Dogs-United States, 2006-2016. Zoonoses Public Health. 66(4):417-421.

 Mörner, T. (1992). The Ecology of Tularaemia. Revised Science and Technology, 11(4):1123–1130.

Nakao, J.H., Collier, S.A., Gargano, J.W. (2017). Giardiasis and Subsequent Irritable Bowel Syndrome. A longitudinal Cohort Study using Health insurance Data, Journal of Infectious Diseases, 215(5): 798-805.

Nelson, C.A., Meaney-Delman, D., Fleck-Derderian, S., Cooley, K.M., Yu, P.A., and Mead, P.S. (2021). Antimicrobial Treatment and Prophylaxis of Plague: Recommendations for Naturally Acquired Infections and Bioterrorism Response. MMWR Recommendation Report.70(No. RR-3):1–27. 

Office International des Épizooties. (2000). Manual of Standards for Diagnostic Tests and Vaccines: Lists A and B Diseases of Mammals, Birds and Bees. Paris, 494–496.

Pearson, A. (1998). Zoonoses: Biology, Clinical Practice, and Public Health Control (Soulsby EJ, Palmer S.L .eds.). Oxford University Press, 276–279.  

Rapini, R.P., Bolognia, J. L. and Jorizzo, J. L. (2007). Dermatology Vol. (2), St. Louis, Mosby. 

Ryan K.J and Ray, C.G. (2004). Sherris Medical Microbiology (4th Ed.). McGraw Hill, 488–90. 

Tarnvik, A. (2007).  WHO Guidelines on Tularaemia. pdf icon (PDF – 125 pages) Vol. WHO/CDS/EPR/2007.7. Geneva: World Health Organization.

Todar K. Mycobacterium Tuberculosis and Tuberculosis Textbook of Bacteriology.net. Retrieved 24th January, 2023.

Trevisanato, S. I. (2007). The Hittite Plague. An Epidemic of Tularemia and the First Record of Biological Warfare, Medical Hypotheses, 69(6):1371-1374.

Vaheri, A., Vapalahti, O., and Plyusnin, A. (2007). How to Diagnose Hantavirus Infections and Detect them in Rodents and Insectivores. Review of Medical Virology,18:277–288.

Weber, I.B., Turabelidze, G., Patrick, S., Griffith, K.S., Kugeler, K.J., and Mead P.S. (2012).  Clinical Recognition and Management of Tularemia in Missouri: A Retrospective Records Review of 121 Cases. Clinical Infectious Diseases, 55(10):1283-1290.

WHO (2021). Common Wild life Diseases Fact Check via www.who.int/news-room/fact-sheets/details/disease. Retrieved on 21st June, 2021.