Neglected Bacterial and Parasitic Zoonoses of Tropical Countries

Abstract

Approximately 60% of human infectious diseases are zoonotic. Many of these zoonotic diseases are endemic in developing countries, adversely impacting people’s health and livelihood. Most of these endemic zoonoses are neglected because they affect explicitly the socioeconomically poor communities. Due to the endemic status, the diseases are often underreported and remain highly neglected. Despite knowing the fact that neglected zoonotic diseases (NZDs) add to a substantial socioeconomic burden of a country, it is difficult to assess the mortality and morbidity caused by the lack of diagnostic facilities, poor surveillance, inadequate veterinary or medical care, and at times underreported owing to undifferentiated clinical symptoms. However, most of these NZDs are preventable; hence, awareness of their epidemiology, transmission, prevention, and control measures is fundamental. Some of the critically neglected zoonotic diseases, such as anthrax, bovine tuberculosis, brucellosis, leptospirosis, cysticercosis, echinococcosis, toxoplasmosis, and trichinellosis, are discussed in this chapter

1. Introduction

1.1 Synonyms

Charbon, Ragpicker’s disease, Splenic fever, Woolsorter’s disease.

1.2 Etiology

Anthrax is caused by Bacillus anthracis, a rod-shaped, Gram-positive, nonmotile, capsulated, aerobic, or facultatively anaerobic, spore-forming bacterium [1]. The bacterium sporulates after getting exposed to free oxygen. Robert Koch (1876) established Koch’s postulates by cultivating a pure culture of B. anthracis in vitro and inducing anthrax in animals. Also, the first bacterial vaccine was prepared against anthrax by Louis Pasteur (Table 1).

SN	B. anthracis strains	Isolated from and/or used as	Location	Ref.
1	Strain 836	Weapon by USSR	Kirov in 1953	[2]
2	Ames strain	Dead cow	Texas, USA, in 1981	[3]
3	Sterne strain	Avirulent, toxigenic strain for vaccine production	Canada	[4]
4	Vollum	Isolated from cow and used for bioweapon trials in 1942 on Gruinard Island	Oxford, England	[5]

Table 1.

The strains of Bacillus anthracis with different evolutionary histories or origins.

1.3 Epidemiology

B. anthracis has a wide geographical distribution. It caused the death of 30,000–60,000 animals in 1923 in South Africa due to this disease [6]. While in North America, Western Europe, and Australia, anthrax is reported sporadically. Anthrax is absent in northern and central Europe; however, enzootic occurrence has been documented in Greece, Spain, Southern Italy, Turkey, and Albania, whereas it is endemic in Asia, including eastern India, South Korea, the Philippines, Mongolia, and the mountainous region of western China [1, 7]. The outbreaks in African countries occur every summer with increased years of heavy rainfall [1, 7]. Anthrax spores are the potential bioterrorism agent which resulted in five deaths and the suffering of 30,000 people in the USA in 2001 [1].

1.4 Host range and reservoir

Soil, fodder, bone meal, infected excreta, blood, and infected discharges are the potential reservoirs of anthrax bacilli. The bacilli spread through contaminated streams, insects, and feces of infected birds, feral cats, dogs, and other carnivores [7]. Compared to sheep and goats, cattle are more frequently infected as they ingest higher doses of bacilli from contaminated soil as cattle graze by pulling pasture out of the ground with roots. In contrast, sheep and goats browse plants and shrubs off the ground level [8]. Anthrax occurs less frequently in horses, pigs, and dogs, whereas cats are relatively resistant. Anthrax is mainly transmitted to herbivores by ingesting contaminated fodder or improperly processed feed and inhaling spores. Carnivores and omnivores can become infected through ingestion of infected carcasses or contaminated meat, as well as direct contact with body secretions or contaminated fomites. Direct animal-to-animal transmission is rare, and there is no evidence of transmission through milk. Direct exposure to anthrax spores is necessary for the disease to occur, which can happen through contact with infected animals during agricultural or animal husbandry operations, handling of animal carcasses, or inhalation of spores in dust clouds created from handling animal products like hides, skins, bone, blood meal, and meat meal.

1.5 Pathogenesis

B. anthracis possesses two important virulence factors, the capsule and the toxin complex, encoded by plasmids pXO2 and PXO1. The capsule helps the bacterium evade the host immune system and establish itself in host tissues, while the toxin complex comprises three lethal proteins to the host. Anthrax outbreaks have been associated with significant climate changes, such as heavy rain after a prolonged drought or warm weather [7, 9]. Sporulation of B. anthracis occurs rapidly when the environmental temperature is over 53°F (12°C) [10]. Anthrax spores have a high surface hydrophobicity, leading to their clumpy, concentrated nature in standing water and concentration on soil surfaces after the water evaporates. These relationships between anthrax and climate may help predict anthrax years [7, 9].

1.6 Disease

1.6.1 Disease in animals

Infected animals exhibit congestion, hemorrhages, high fever, dyspnea, edema, depression, anorexia, convulsions, staggering gait, diarrhea/dysentery, abortion, blood-stained milk, and absence of rigor mortis. In herbivores, the disease is primarily hyperacute and fatal, with sudden death occurring within 10–24 h due to septicemia and toxemia. The gastrointestinal form is the most common. Cutaneous anthrax can occur in animals through the bite of mechanical vectors or wound contamination, but death usually occurs before eschars/carbuncles develop. The disease can be fatal in carnivores, or the animal can recover. Intestinal form is occasional, and death is due to airway occlusion. Carbuncular lesions may develop on the tongue or oropharynx.

1.6.2 Disease in man

Human anthrax has a variable incubation period (usually 2–5 days) which is potentially fatal.

• Cutaneous form (malignant pustule/eschar): The spores enter through cuts or abrasions in the skin and form a papule which becomes necrotic and later ruptures to painless black eschar or carbuncle (that resolves within 2–6 weeks) surrounded by an edematous zone. The secondary bacterial infection leads to pus formation. In septicemic cases, symptoms include fever (40°C), chills, headache, nausea, anorexia, dyspnea, cyanosis, and collapse preceding death.

• Pulmonary form (Woolsorter’s disease): The spores enter through inhalation while handling raw wool, hides, bones, blood meal, and meat meal. Symptoms include fever, dyspnea, pneumonia, emphysema, and cardiac failure. The septicemic complication is highly fatal.

• Intestinal form: Characteristic eschar or malignant carbuncle occurs on the oropharynx, stomach, duodenum, and upper ileum. The spores enter by ingesting infected meat, milk, or other foodstuffs. The symptoms include nausea, vomiting, anorexia, fever, abdominal pain, watery to bloody diarrhea, and tenderness in the right upper and lower quadrants.

1.7 Diagnosis

In the case of an animal suspected of dying of anthrax, the carcass should not be opened to prevent contamination of the surrounding area with spores. If the carcass has been mistakenly opened, the dark unclotted blood and massive hemorrhagic spleen will be visible. A quick and reliable diagnosis can be made by staining blood smears from ear clippings (in all animals, including wild animals), laryngeal edema (in dogs and pigs), or mesenteric lymph nodes (in sheep, goats, cattle, and horses) with polychrome methylene blue; the bacterial capsule appears reddish-purple on microscopic examination, while the bacilli take up a deep blue color. The pathogen can be isolated from clinical material on blood agar to study the characteristic morphology of bacilli and the “medusa head” appearance of colonies. Laboratory animals, such as guinea pigs (subcutaneous (s/c)) and mice (intraperitoneal (i/p)), can be inoculated with clinical material (0.5 ml) to confirm Koch’s postulates and the pathogenicity of the bacilli (death of the animal by pathogenic bacilli occurs within 30–40 h of inoculation). Ascoli’s precipitation test uses anthrax hyperimmune serum against attenuated anthrax spores to detect residual anthrax antigens in tissues/hides. Polymerase chain reaction (PCR) can detect even a single cell of B. anthracis and differentiate it from other closely related species.

1.8 Treatment

Penicillin (V or G) is the drug of choice for 5–7 days by oral, intramuscular (i/m), or intravenous (i/v) route. Streptomycin may also act synergistically with penicillin. Other drugs used are tetracycline, gentamicin, erythromycin, and chloramphenicol.

1.9 Prevention and control

It is crucial to interrupt the infection cycle by stopping the source of infection. Contaminated feed and the source of infection should be promptly disposed of. The introduction of new animals to the affected farms should be prevented. If insects (flies) are believed to be spreading the disease, measures should be taken to control their population [11]. In cases where there is a delay in the disposal of the anthrax carcass and infected materials, applying 5% formaldehyde and covering the area with double-thickness plastics are recommended. The formalin-treated carcass can be left in place for a few days before disposal, as it will maintain an anaerobic environment inside. Special attention is required to disinfect areas or items contaminated with anthrax, such as floors, rooms, fertilizers, meat, hides, and wool. Regular disinfectants or heat (60°C for a few minutes) can eliminate the vegetative form of bacteria shortly after the animal has died. Strong disinfectants like Peracetic acid (3% solution), 5% Lysol, formalin, or sodium hydroxide (5 to 10%) are helpful. Dirty shoes can be disinfected with ethylene oxide, while hides and wool can be sterilized by gamma irradiation. Contaminated clothes should be treated with 10% formaldehyde. If human skin is contaminated, the affected area must be disinfected [7]. The live attenuated B. anthracis strain Sterne 34F2 vaccine is the most effective vaccine against anthrax in animals. Vaccination should be done 2–4 weeks before a potential anthrax outbreak, followed by a second dose 2–4 weeks after the first dose. Suppose anthrax cases are detected in a specific area for the first time. In that case, animals that have come into contact with the infected ones should be treated with hyperimmune serum or vaccinated. Typically, after the vaccination of cows, the milk should not be consumed for 72 h, and the animals are not slaughtered for 45 days. Human anthrax cases should be promptly treated, and the disease should be notified to local health authorities.

2. Brucellosis

2.1 Synonyms

(In man: Undulant fever, Malta fever; In animals: Contagious abortion, Infectious abortion, Epizootic abortion; In cattle: Bang’s disease; and In male sheep: Ram epididymitis).

2.2 Etiology

Brucella genus belongs to the α-2-Proteobacteriacae family, which is responsible for causing Brucellosis in both animal and human species. These Gram-negative, intracellular nonsporulating coccobacilli are aerobes, but some species require 5–10% carbon dioxide (CO2) for survival. Out of the recognized Brucella species, seven are terrestrial (Brucella abortus, Brucella melitensis, B. suis, Brucella ovis, B. canis, Brucella neotomae, and Brucella microti) [12, 13], while two are marine (Brucella ceti and Brucella pinnipedialis) [14, 15]. In addition, three new species (Brucella inopinata, B. papionis, and B. vulpis) have been isolated from human breast implants, baboons, and red foxes, respectively, and a new lineage of Brucella (BO2 strain) has been identified [16]. Besides, 36 atypical Brucella species have been isolated from frogs [17, 18].

2.3 Host range and epidemiology

Brucella organisms can be found in cattle, buffaloes, sheep, and goats. Cattle and buffalo are the primary hosts for B. abortus, but under certain conditions, Brucella species can cross the species barrier and infect new susceptible hosts [19]. This interhost transmission seriously threatens public health, particularly with the highly virulent and zoonotic B. melitensis and B. suis strains. B. ovis can infect sheep, but the infection does not typically last long in ewes and gets eliminated before the next lambing [20]. Swine brucellosis is primarily a problem in domesticated pigs, caused by Brucella suis, and can lead to chronic reproductive issues in both sexes.

2.4 Transmission

• In animals: Bovines catch an infection while grazing on contaminated pastures or barns. Infection can also transmit via contact with infected animals, ingesting contaminated feed, fodder, and water, or through uterine secretions and aborted materials. Using infected milking cups, feeding pooled colostrum to newborn calves, and artificial insemination can also contribute to the spread of the disease. Bringing infected animals into a healthy herd can also introduce the risk of infection. In sheep and goats, brucellosis is highly contagious due to close contact in dense flocks, mingling at animal fairs, overcrowding in winter, and exposure to different flocks from different owners. B. suis can survive for long periods in hog lots and furrowing pens, increasing the risk of transmission. In India, the spread of the disease has been attributed to a lack of vaccination for female calves, a ban on cow slaughter, and a lack of awareness about protective measures.

• Humans: Humans are at risk of contracting brucellosis, typically through handling infected animal tissues and body fluids, consuming raw milk and milk products, or inhaling contaminated aerosols.

2.5 Pathogenicity

The ability of Brucella species to cause disease is determined by its capacity to adhere to, invade, and replicate within host cells. Brucella bacterium can prevent phagosome-lysosome fusion and spread to other host cells. It causes chronic infections by prolonged survival and replication in phagocytic macrophages or acute reproductive tract pathology and abortion by extensive replication in nonphagocytic epithelial cells, such as placental trophoblasts, in natural animal hosts. In humans, Brucella colonizes different organs, with a preference for the lymphoreticular system. The disease is more apparent in adults and pregnant animals than young animals of either sex because a concentration of sex hormones and erythritol sugar increases with age and sexual maturity, which are required for the growth and multiplication of the Brucella pathogen.

2.6 Disease

2.6.1 Disease in animals

Bovine brucellosis is a longlasting infection with B. abortus causing abortion, infertility, repeat breeding, retention of placenta, stillbirth, epididymitis, and orchitis. Asymptomatic bovines play a significant role in maintaining a hidden infection within a herd. Asymptomatic females become carriers after the first abortion and transmit the infection to other healthy animals. Among small ruminants, goats are more susceptible than sheep, as they can excrete the organism for a more extended period. Lactating ewes are also more susceptible to infection than sheep raised for meat [21]. In female sheep and goats, brucellosis causes abortion during the last trimester of pregnancy, weak offspring, and retention of fetal membranes. In males, acute orchitis, epididymitis, and infertility can occur. Carrier males can spread the infection through semen, as the bacteria can be present in their testicles, epididymis, and secondary sex organs. Arthritis has been reported in both sexes, but it is not shared. Males are less susceptible to infection than females due to the lower concentration of erythritol sugar in their bodies [22]. Infected boars carry bacteria in semen, becoming a transmission source [23].

2.6.2 Brucellosis in humans

The most common symptoms are undulant fever, joint pain, and night sweats. Other symptoms may include spondyloarthropathy, epididymal-orchitis, infertility, spondylitis, acute polyarthritis, upper and low back pain, and fatigue. In rare cases, Brucella infection may lead to abortion in pregnant women. Children with brucellosis may experience joint pain, low backache, fatigue, and night sweats. Neurobrucellosis is a severe disease that affects the nervous system, can occur untreated, and may even cause transient ischemic attacks [24].

2.7 Diagnosis

Animals are typically screened for brucellosis using the Rose Bengal Plate Test (RBPT) and the serum tube agglutination test (STAT). A positive test in small ruminants is considered when agglutination occurs at a titer of 1:20 (40 international units (IU)) or higher. According to the Centers for Disease Control and Prevention (CDC), a titer of 1:80 or greater is clinically significant in humans. However, a 4-fold or greater increase in titer between acute and convalescent phase sera is required to diagnose acute infection. The complement fixation test (CFT) is a recommended test for brucellosis control and surveillance programs and for international trade [25]. Enzyme-linked immunosorbent assay (ELISA) is a sensitive and rapid method for diagnosing brucellosis, with the added advantage of diagnosing the disease in both endemic and low-incidence areas. The Milk Ring Test (MRT) is a rapid agglutination test that detects immunoglobulins such as immunoglobulin M (IgM) and immunoglobulin A (IgA) attached to fat globules in whole milk or cream. It is the method of choice in dairy herds for inexpensive screening of individual or pooled milk samples in conjunction with other tests. The 2-mercaptoethanol serum tube agglutination test (2ME-STAT) and Coombs test are other critical diagnostic tests for detecting immunoglobulin G (IgG) antibodies in chronic brucellosis cases. Molecular techniques such as polymerase chain reaction (PCR) are promising methods for rapid and accurate diagnosis of brucellosis.

2.8 Treatment

Animals infected with brucellosis cannot be effectively treated, and treatment is not recommended. For humans, the recommended treatment is a combination of rifampicin and doxycycline, taken once daily for 6 weeks.

2.9 Prevention and control

The test and slaughter of positive animals successfully eradicate brucellosis in many developed countries. However, it is not a feasible option in developing countries like India due to the economic loss it would cause to farmers and due to the cultural and religious significance of cattle. In place of this, vaccination, test, and quarantine policies, improved housing practices, proper disposal of infected materials, thorough disinfection of contaminated animal premises, and mandatory calf hood vaccination are recommended. The World Organization for Animal Health (OIE) has recommended the Brucella S19 and RB51 vaccines for the prevention of bovine brucellosis, with the RB51 vaccine having been successfully used in the United States since 1996. Positive bulls should be culled and segregated. It is essential to avoid consuming undercooked and unpasteurized milk and milk products, and people who handle animal tissues should use protective gear such as rubber gloves, goggles, gowns, or aprons.

3. Bovine tuberculosis

3.1 Synonyms

Great white plague, Pearl disease, Scrofula, Tuberculous, caseous pneumonia.

3.2 Etiology and pathogenicity

Mycobacterium bovis is part of the Mycobacterium tuberculosis complex (MBTC), which also includes other species such as Mtb, M. caprae, M. microti, M. africanum, M. canettii, Mycobacterium pinnipedii, M. bovis, Mycobacterium leprae, and M. mungi. Mycobacteria are aerobic, nonmotile, noncapsulated, nonspore-forming, and have straight or slightly curved rods. The survival of tubercle bacilli in the environment differs greatly depending on temperature, sunlight, and relative humidity, ranging from a few days to 2 years. M. bovis can be inactivated by heat, direct sunlight, and dry conditions. They can be killed at a temperature of 65°C or higher for at least 30 min and by ultraviolet (UV) light. However, M. bovis (M. bovis) is resistant to prolonged freezing and can persist in slurry and soil for at least 6 months at ordinary temperatures [26]. Mycobacterium are known to be resistant due to their high lipid content to several chemicals and disinfectants. While quaternary ammonium compounds, hexachlorophene, and chlorhexidine can have a bacteriostatic effect on it, formaldehyde vapor, chlorine compounds, 70% ethanol, hydrogen peroxide, alkaline glutaraldehyde, and 5% phenol are effective in killing the bacteria. M. bovis are highly pathogenic mycobacteria that cause TB in humans and animals. M. bovis is the leading cause of TB in cattle [27].

3.3 Epidemiology

Developed countries have controlled the spread of the disease in cattle by implementing test-and-slaughter control programs. In contrast, bovine tuberculosis (bTB) continues to be widespread in developing countries such as India, where humans and cattle live close to each other, and unpasteurized milk consumption is typical. Mycobacterium orygis (M. orygis) is a new subspecies of the M. tuberculosis complex (MTBC) that causes tuberculosis in animals and humans and has been reported in several countries, including India, Pakistan, Bangladesh, and Nepal [28, 29, 30, 31]. In 2016, 147,000 new cases of zoonotic TB and 12,500 deaths were reported globally [32].

3.4 Host range and reservoir

M. bovis and M. tuberculosis belong to the M. tuberculosis complex (MTBC). M. bovis causes bovine tuberculosis (bTB) in animals, while M. tuberculosis causes tuberculosis (TB) in humans [33]. Cattle are the primary carriers of M. Bovis. Besides cattle, goats, pigs, buffalo, dogs, primates, badgers, deer, possums, and bison can also serve as reservoirs of M. bovis.

3.5 Transmission

Ingestion of raw milk is the primary transmission route of M. bovis from cattle to humans. Individuals working in close contact with livestock are at risk of transmitting infection between cattle and humans and vice versa. Inhalation of cough droplets from infected cattle causes a typical pulmonary TB [34, 35, 36, 37].

3.6 Disease

3.6.1 Disease in cattle

The superficial lymph nodes are usually swollen in infected animals. The affected udder progressively becomes more rigid and swollen. The milk of infected animals is thin and watery with yellow flakes. Chronically infected animals become emaciated, with a dry and rough coat, sunken and dull eyes, diarrhea, unpredictable appetite, and fluctuating body temperature. In some cases, the animal may snore due to the involvement of the retropharyngeal lymph node. In cases of cutaneous TB, there may be lumpy swelling, sometimes with cording, on the lower part of the front legs and rarely on the hind legs.

3.6.2 Disease in man

Clinical tuberculosis occurs in three stages in humans.

• Primary tuberculosis: Lung infection leads to the formation of tubercles with center-containing bacteria. When the center of the tubercle breaks, it turns into a necrotic, cheese-like substance called a caseous lesion, but eventually, it may heal and harden by forming calcium deposits.

• Secondary tuberculosis: Inactive bacteria in the primary infection become active again, producing chronic tuberculosis. The bacteria move to the upper respiratory tract and bronchial tubes, causing severe coughing, fever, weight loss, anorexia, fatigue, chest pain, and greenish or bloody sputum production.

• Extrapulmonary tuberculosis: In secondary tuberculosis, the bacteria spread quickly to other body parts such as the lymph nodes, kidneys, long bones, genital tract, brain, and meninges. Renal tuberculosis can lead to tissue death and scarring in the kidneys, pelvis, ureters, and bladder. Genital tuberculosis impacts reproductive functions in males and females. Tuberculosis in bones and joints, especially the vertebral column, can result in loss of sensation and paralysis. Tuberculous meningitis can cause mental deterioration, permanent mental retardation, blindness, and deafness. M. bovis can cause a condition called scrofula in children. It occurs when the infection spreads to the cervical and, less commonly, axillary lymph nodes, primarily through ingestion of contaminated food.

3.7 Diagnosis

Isolation and identification of the pathogen remain the only confirmatory test, but the growth of M. bovis may take 6–8 weeks. In animals, the histological examination of the tubercle from suspected animals or carcasses enables rapid diagnosis of acid-fast bacilli. Delayed-type hypersensitivity (DTH) assays, such as Single intradermal tuberculin, Stormont, and Short thermal tests, are helpful. Inoculation of suspected milk samples into the thighs of guinea pigs produces typical lesions in the liver, spleen, and lymph nodes. Multiplex PCR and gamma-interferon (IFN-γ) assays are more sensitive than skin tests but are costly. A combination of intradermal skin test (ST) and ELISA has enhanced sensitivity compared to individual tests. In humans, chest X-rays, roentgenographs, and the Mantoux test have diagnostic importance.

3.8 Treatment

In men, tuberculosis (TB) is a treatable disease that is usually controlled with a 6-month duration of antibiotics, like rifampicin and isoniazid. However, drug-resistant TB requires longer and more complex treatment. Compared to the traditional 6 months, treatment options have been shortened to only 1 or 3 months.

3.9 Prevention and control

• In animals: The test-and-slaughter policy is the most effective method to eradicate bTB, but it is only feasible in developed countries. Due to public and religious issues, a test-and-slaughter policy may not be possible in India. Good surveillance and reporting systems are essential for screening and controlling bovine TB in animal populations. The sanitary inspection of carcasses at abattoirs can reduce transmission at the animal-human interface. Animal sheds should be spacious and ventilated to avoid transmission of infection between animals. Establish reference laboratories to confirm diagnosis and research on the potential role of other domestic and wild animals as disease reservoirs and vaccination.

• In man: Condemnation of milk from infected herds, regular health checks for occupational groups at risk, such as butchers and farmers regarding M. bovis, promotion of milk pasteurization, health education, effective implementation of BCG vaccination, and preventive chemotherapy.

4. Leptospirosis

4.1 Synonyms

Cane cutter’s disease, Harvest fever, Infectious jaundice, Mud fever, Rice field worker’s disease, Seven-day fever, Swamp fever, Swine herd’s disease, Weil’s disease

4.2 Etiology

Leptospirosis is caused by Leptospira interrogans (L. interrogans) complex, which has over 20 serogroups and more than 200 serovars. Previously, all saprophytic species of Leptospira were classified under Leptospira biflexa, while L. interrogans were referred to as all pathogenic species [38, 39]. Leptospirae are small, highly motile, thin, flexible, and filamentous, made up of delicate spirals with hook-shaped ends. Leptospirae cannot survive in dry environments, heat, acids, and primary disinfectants but can sustain alkali pH up to 7.8. This bacterium can only be visualized with silver impregnation staining, immune peroxidase staining, or immunofluorescence under a dark field microscope (Table 2).

Serovar	Maintenance host	Incidental host
L. bratislava	Pig	Horse, Dog
Leptospira canicola	Dog	Pig, Cattle
L. grippotyphosa	Rodent	Cattle, Pig, Horse, Dog
L. hardjo	Cattle	Human
L. interohemorrhagie	Brown cat	Domestic animals and human
L. pomona	Pig, Cattle	Sheep, Horse, Dogs

Table 2.

Maintenance and incidental hosts for important serovars of Leptospira interrogans [40].

4.3 Epidemiology

Leptospirosis has high incidence rates in Southeast Asia, Oceania, the Indian subcontinent, the Caribbean, and Latin America [41]. The occurrence of the disease is significantly affected by changes in climate, flooding, inadequate sanitation, and the presence of reservoir hosts such as rats. The annual incidence in these regions can range from 10 to 100 cases per 100,000, which increases during outbreaks and in high-risk populations [42]. In recent years, there have been changes in the epidemiology of leptospirosis, with sporadic outbreaks occurring in nonendemic regions such as Canada, continental USA, and Europe, often associated with water-sport activities in natural settings contaminated with pathogenic leptospires [41, 43, 44, 45] or changing climatic patterns [41], in recreational settings such as adventure races [45], endurance events [46], and water-sporting events. Leptospirosis is considered a waterborne disease in the Asia-Pacific region, and the outbreaks in Indonesia (2003), India (2005), Sri Lanka (2008), and the Philippines (2009) have been linked to major urban flooding [42, 47]. Lack of proper sanitation and climatic conditions contribute significantly to human leptospirosis. The disease is also prevalent in rural areas, where agricultural activities such as farming and animal husbandry are potential risk factors.

4.4 Transmission

Leptospirosis is primarily transmitted through contact with the urine of infected animals or through contact with skin abrasions. Moist and damp areas, such as riverbanks or muddy livestock-rearing areas, are most likely to carry the bacteria. It is speculated that leptospirosis is transmitted through the semen of infected animals. Humans are accidental hosts, typically becoming infected through direct or indirect contact with infected animals, tissues, body fluids, or urine of acutely infected or asymptomatic carrier animals. Animal carriers and environmental sources play an essential role in the transmission of leptospirae.

4.5 Host range and reservoirs

Leptospirosis primarily infects animals, but humans are “dead-end” hosts. The disease has been reported in domestic animals (cattle, buffalo, sheep, goats, pigs, and horses), wild animals (elephants, deer, and monkeys), and rodents (rats, mice, bats, rabbits, hares, and squirrels). Carnivores (dogs, cats, jackals, foxes, mongooses, skunks, civets, and raccoons) and porcupines, insectivores, and frogs may also carry leptospirae. Birds, including domestic poultry, are resistant to the disease; wading birds can act as passive carriers of the infection. Infected rodents and mammals are the primary natural reservoirs of the disease, with the pathogen surviving and being shed in urine, particularly in herbivores. The pathogen can survive for weeks in soil and water frequently contaminated by urine from carriers, particularly in alkaline pH conditions. Fish, reptiles, and birds have also been identified as potential disease carriers.

4.6 Disease

4.6.1 Disease in animals

The symptoms and severity of the disease can vary depending on the animal species.

• Cattle: In the acute form of the disease, cattle may show a sudden onset of fever, anorexia, jaundice, anemia, hemoglobinuria, depression, and abortion during the third trimester of pregnancy. In the subacute form, “milk drop syndrome” is expected due to mastitis resulting in reduced milk yield, thick flaking, and yellow-to-blood coloration of milk. Chronic cases may result in abortions, stillbirths, weak calves, and retained placenta cases.

• Swine: Leptospirosis in swine is usually mild or inapparent, with only one or a few affected pigs showing acute signs of anorexia, fever, and diarrhea. Chronic cases may result in late pregnancy abortion or weak piglets that usually fail to survive and recover but become renal shedders for at least 6 months.

• Dogs: Leptospirosis can cause elevated body temperature, depression, deep sunken eyes, anorexia, muscle tenderness, vomiting, intussusception, foul breath, ulcerated gums, and extensive jaundice that may lead to death. The acute form of the disease, known as “Stuttgart disease,” is characterized by vomiting, rapid dehydration, collapse, necrosis, and sloughing of the buccal mucosa and tongue, the occasional passage of blood-stained feces, and high mortality.

• Horses: Leptospirosis in horses is rare and usually mild, but it can cause pyrexia, icterus, periodic ophthalmia, and abortion.

• Sheep: The common signs include abortion, fever, agalactia, dyspnea, jaundice, hematuria, and sudden death.

• Goats: Mostly asymptomatic but shed leptospires in the urine for short periods or may develop jaundice, hemoglobinuria, and abortions.

4.6.2 Disease in man

The disease is manifested in two phases after an incubation period of 7: 12 days

• Early or Leptospiaremic phase: The disease is manifested as a flu-like illness characterized by abrupt onset of high fever, chills, headache, muscle pain, vomiting, and eye redness. Most individuals recover fully from the mild form, even without medication. Untreated infection may progress to the second stage.

• Second or Immune phase/Weil’s syndrome: Untreated disease worsens to kidney and liver failure. Jaundice results from liver failure. Anemia occurs due to widespread hemorrhages, which can lead to coma and death, particularly in older patients or with more virulent strains of the disease. Conjunctival suffusion, “red eye,” is a constant and unique symptom. In rare cases, severe forms of the disease may present as atypical pneumonia, aseptic meningitis, or myocarditis. The mortality rate of severe forms ranges from 5 to 10%, which is significant.

4.7 Diagnosis

A tentative diagnosis of the disease can be made based on the clinical symptoms that suggest possible infection, especially in individuals from high-risk groups and endemic areas. However, a confirmatory diagnosis is necessary and can be made as follows

4.7.1 Direct examination of samples

Microscopic techniques, such as dark field microscopy (400x) and silver staining, can visualize leptospires in impression smears or tissue sections.

4.7.2 Isolation of leptospires

Conventional methods for detecting leptospires in clinical or pathological materials, especially blood, include culture, animal inoculation, and culture following animal inoculation.

1. Culture: The isolation rate of leptospires from clinical specimens such as blood, urine, cerebrospinal fluid (CSF), kidney, liver, and brain from aborted fetuses, uterine swabs from abortion cases, and semen is shallow. Media for culturing leptospires are media containing serum (Korthof’s medium, Stuart’s medium, and Fletcher’s semisolid medium), media containing bovine albumin fraction V and Tween 80 (EMJH (Ellinghausen-McCullough-Johnson-Harris) medium, protein-free medium, Ellis medium), and chemically defined media (Burgess medium and T80 medium).

2. Animal inoculation: It is carried out to increase the concentration of Leptospira cells. In gerbils, a 10⁶ leptospire inoculum usually induces a fatal reaction in 3–5 days. Inoculation of a hamster (3 weeks old) with 0.5⁻¹ ml of a sample through the intraperitoneal route induces jaundice, resulting in a fatal infection. Leptospires can be recovered from guinea pigs (1 week old) that died after 21 days of inoculation with 0.5⁻¹ ml of the infected material through the intraperitoneal route.

4.7.3 Common serological diagnostic tests

1. Microscopic agglutination test (MAT): MAT is the World Health Organization (WHO) standard reference test for the fast, specific, and routine diagnosis of leptospirosis. It employs mixing equal volumes of a series of serum dilutions and either live or formalized Leptospira culture. A titer of 1:100 or more indicates present or past infection, and the titer may be higher in vaccinates.

2. Macroscopic agglutination test: This test is similar to the MAT, but the agglutination reaction is visible to the naked eye. It is less sensitive than the MAT and is not recommended for routine diagnosis.

3. Enzyme-linked immunosorbent assay (ELISA): This test is highly sensitive and specific and can detect IgG and IgM antibodies separately.

4. The indirect hemagglutination (IHA) test: This test involves sensitizing sheep or human red blood cells with Leptospira antigens, which agglutinate antibodies in the test serum. A positive result is indicated by an agglutination reaction equivalent to 2+ or more.

5. Complement fixation test (CFT): This test involves inactivating the serum and titrating the complement in the presence of antigen to be used in the test. A positive result is indicated by reduced complement activity due to antibodies in the serum.

6. The sensitized erythrocyte lysis (SEL) test: This test involves mixing twofold dilutions of test serum with sensitized sheep erythrocytes and complement and observing for hemolysis in the presence of complement.

7. Other tests that may be used include the growth inhibition test (GIT), immunoperoxidase test, chemiluminescent test, and DNA hybridization with biotin-labeled leptospiral DNA.

4.7.4 Diagnostic tests for rapid or early detection

Several other sensitive and specific tests are available for detecting leptospires. However, they are not routinely used as they are more complex or expensive than conventional methods and may require specialized equipment or expertise. These include the Immunofluorescence test, Polymerase chain reaction (PCR), Microcapsule agglutination test (MCAT), Radioimmunoassay (RIA), Passive hemagglutination (PHA) test, and Rapid microscopic agglutination test (RMAT).

4.8 Treatment

Antibiotic treatment should be initiated as soon as possible once symptoms appear. Ampicillin, doxycycline, erythromycin, penicillin, tetracycline, and streptomycin can treat leptospirosis. Treatment and vaccination of beef herds are recommended to prevent abortion. While in dairy cattle, only infected animals should be treated to prevent the spread of infection.

4.9 Prevention and control

The risk of leptospirosis can be reduced by avoiding water contaminated with animal urine or contact with infected animals, proper draining and cleaning of yards, pens, sheds, and kennels with cresol or sodium hypochlorite (1:4000), avoidance of stagnation of water, urine, and feces, and burial or burning of infected carcasses, aborted fetuses, placentas, and bedding. Occupational workers should wear protective clothing or footwear. Any skin cuts should be covered with waterproof dressing while swimming in freshwater. Preventing rodents from invading residential areas and water sources reduces the risk of infection. Vaccination against the bacteria can protect pet dogs and the household from leptospirosis, while human immunization provides a certain degree of protection. Available vaccines for domestic animals can decrease the severity of the disease, although they cannot provide complete protection as the immunity is serovar-specific. Pigs are typically vaccinated every 6 months, while annual vaccination is usually sufficient for dogs, cattle, and sheep. Proper quarantining and testing new animals before introducing them to a herd or flock would help remove carrier animals. Educating the general public, especially high-risk groups, about leptospirosis and avoiding recreational activities in contaminated water are necessary for disease prevention.

5. Hydatidosis

5.1 Etiology

The adult tapeworms (cestode) of Echinococcus granulosus and Echinococcus multilocularis occur in the small intestine of canids (definitive host). Larval stages of E. granulosus (hydatid) and E. multilocularis (metacestode) occur in tissues of the liver, lung, and other organs of other mammals (intermediate host), including humans. Infection with the larval stages of E. granulosus in, the intermediate host, causes “cystic echinococcosis” or “hydatidosis,” which causes significant economic losses and public health issues. In contrast, infection with metacestode causes severe disease, referred to as “alveolar echinococcosis.”

A hydatid cyst is a big sac filled with liquid and lined by germinal epithelium, which produces small scolices that are either separate or clumped together in brood capsules. Anything inside the cyst other than the liquid, such as the scolices and brood capsules, is sometimes called “Hydatid Sand.” If the cyst wall breaks open from the outside, hydatid sand can also form inside the cyst [48]. The fluid inside a hydatid cyst is typically pale yellow and contains 17–200 mg of protein per 100 ml. The hydatid cyst has an outer connective tissue covering beneath the germinal epithelium. Both large and daughter cysts contain germinal layers from which scolices develop. Each protoscolex can grow into one adult tapeworm in the final host.

5.2 Life cycle

An adult tapeworm of E. granulosus passes eggs in the feces of the definitive host (Canids). Eggs hatch in the small intestine of an intermediate host when ingested through contaminated feed and water. Hatched eggs release six-hooked oncospheres that penetrate the intestinal wall and migrate through the circulatory system into various organs, especially the liver, and lungs, where they develop into a thick-walled hydatid cyst from the oncospheres. When a definitive host ingests organs infested with cysts, the protoscolices evaginate from the cyst and attach to intestinal mucosa to develop into the adult stages in 32 to 80 days, and this slow-growing hydatid cyst usually takes 6–12 months to become an infective mature stage which has two layers: inner germinal epithelium and an outer membrane. Brood capsules detach from the germinal epithelium and exist freely in the hydatid fluid. Daughter cysts are formed inside or outside the mother cyst [48]. The multilocular, unilocular, and sterile cysts are frequently noted in sheep, horses, and cattle. As a thin-walled cyst embedded in the organ grows, it leads to a local reaction, whereas a thick fibrous capsule is formed around the cyst in horses. Humans act as dead-end hosts because dogs do not have access to eat hydatid cysts containing flesh.

5.3 Epidemiology

Hydatidosis is a zoonotic infection that occurs worldwide. It is most commonly found in Mediterranean countries, Southern South America, the Middle East, Iceland, New Zealand, Australia, and Southern Africa. In endemic areas, the incidence of cystic echinococcosis (CE) varies from 1 to 220 cases per 100,000 people, whereas the incidence of alveolar echinococcosis (AE) ranges from 0.03 to 1.2 cases per 100,000 people [49]. In India, the prevalence of E. granulosus infection in the stray dog population varies from 4.35% in Karnataka [50], 33.3% in Andhra Pradesh [51], and 5.22–6.57% prevalence in Maharashtra [52].

5.4 Pathogenicity of human hydatidosis

Echinococcus granulosus causes cystic echinococcosis (CE) while Echinococcus multilocularis (rare, most virulent) produces alveolar echinococcosis [49]. In 63% of echinococcosis cases, cysts have been reported in the liver and 25% in the lungs [49]. The symptoms of cystic echinococcosis in the liver include obstructive jaundice, abdominal pain, rupture of cyst into the abdominal or peritoneal cavity, urticaria, and/or severe anaphylactic reaction due to the pressure effect of the cyst in the liver and due to the presence of cysts in the lungs causes chronic cough, dyspnea, pleuritic chest pain, and hemoptysis. Anaphylaxis due to the rupture of the cyst may lead to death; however, if the person survives, the released daughter cysts may again grow in other parts of the body [48]. The cerebral involvement is signified by headache, dizziness, and diminished consciousness [49].

Intermediate hosts usually show no visible symptoms. Most often, cysts are discovered only at slaughter. Definitive hosts (canids) are also asymptomatic, even in the presence of thousands of adult tapeworms [48].

5.5 Diagnosis

Diagnosis is based on the detection of adult worm segments (three segments, namely tiny rostellum, six-hooked scolices, and the kidney-shaped ovary) and eggs (an oval shape with a thick shell and radial striation (embryophore)) in the feces [53]. Necropsy can reveal tapeworms attached to the small intestine as slender papillae. Intestinal scrapping, sedimentation, and counting techniques at necropsy also detect intestinal E. multilocularis in definitive hosts [54]. Hydatids are rarely suspected in intermediate hosts, and diagnosis is usually postmortem. Imaging tests such as ultrasound, computed tomography (CT) scan, magnetic resonance imaging (MRI), and serological assays such as complement fixation and immunoelectrophoresis are more commonly used in man. The Casoni test is a hypersensitivity reaction that occurs within 15 min after inoculating fluid of hydatid cyst in the suspected individual [53]. Recent diagnostic trends include peroxidase micro-ELISA and Ab-ELISA, which are used for bovine fertile hydatid cysts [53].

5.6 Treatment

There is no specific treatment for hydatid cysts in domestic animals [55]. Praziquantel is a highly effective drug for treating Echinococcus tapeworms in dogs and cats [48]. Surgical removal is the best treatment for hydatid cysts in humans, but the disease can reoccur even after surgery. Anthelmintics like praziquantel, albendazole, and mebendazole effectively treat hydatid cysts in humans [54].

5.7 Prevention and control

Dog deworming, thorough meat inspection, and public awareness are crucial to break the transmission cycle between the definitive and intermediate hosts. Prevent access of dogs to abattoirs. In some countries, purgative anthelmintiics, like arecoline hydrochloride, are used to expel the entire tapeworm from infected dogs [48]. It is crucial to adopt good personal hygiene practices before and after handling food and dog to prevent the transmission of eggs to humans.

6. Taeniasis

6.1 Etiology

Taeniasis/cysticercosis is a neglected tropical disease highly endemic in many sub-Saharan African, Southeast Asia, and Latin American countries. The socioeconomic impact of cysticercosis is immense as it affects the health and livelihood of farming communities by reducing the market value of pigs (and cattle) and rendering pork/beef unsafe for human consumption. Taeniasis is an intestinal infection caused by pork tapeworm (Taenia solium), beef tapeworm (Taenia saginata), and Asian tapeworm (Taenia asiatica).

6.2 Life cycle

Humans are the only definitive host for Taenia tapeworms, whereas cattle serve as an intermediate host for T. saginata, and pigs are the intermediate host for Theridion solium and Torenia asiatica species. Taenia eggs are released in human feces and survive for days to months in the environment. Intermediate hosts catch infection when grazing on pastures/soil contaminated with eggs or gravid proglottids. The animal’s intestinal eggs hatch to produce oncospheres that invade the intestinal wall and reach the striated muscles via blood circulation. The larval form (cysticerci) of Taenia tapeworm encysts in muscles where it remains alive for several years. Infection in humans occurs after consuming raw or undercooked meat infected with tapeworm larvae. The larvae develop into adult tapeworms in the human intestine, attaching themselves to their scolex and residing for years. The mature tapeworms release segments called gravid proglottids, which detach from the worm and are excreted in the feces.

6.3 Epidemiology

The infections in men are subjective to poor personal hygiene, sanitary conditions, food habits, and cooking pattern. These infections are common in regions where people are habituated to eating insufficiently cooked or smoked meat (pork/beef). Eating contaminated raw leafy green vegetables with human excreta containing eggs of T. solium can also cause infection in vegetarians.

6.4 Disease

6.4.1 Disease in man

It is manifested mainly in three forms namely Taeniasis, Cysticercosis, and Neurocysticercosis.

1. Taeniasis: It is an infestation with adult tapeworms. Most people with tapeworm infections have no symptoms or mild symptoms. Patients with T. saginatataeniasis often experience more symptoms than those with T. solium or T. asiatica infections because the T. saginata tapeworm is larger (up to 10 m) than the other two tapeworms (usually 3 m). Symptoms include abdominal pain, loss of appetite, weight loss, nausea, diarrhea, or constipation.

2. Cysticercosis: It is an infestation with larvae/cysticerci. T. saginata does not cause cysticercosis in humans. It is not clear if T. asiatica causes cysticercosis in humans or not. However, infection with T. solium cysticerci can result in human cysticercosis, which causes variable clinical symptoms, including visible or palpable nodules beneath the skin.

3. Neurocysticercosis: It is caused when the larvae of T. solium encyst in the central nervous system (CNS), including the brain. It causes chronic headaches, blindness, and epileptic seizures, and sometimes it can be fatal.

6.4.2 Disease in animals

Signs and symptoms of cysticercosis in pigs (porcine cysticercosis): Typically, there are no symptoms in pigs. At examination, the heavily infected pigs can show cysts on their tongue.

6.5 Diagnosis

Diagnosis in man is based on demonstrating proglottids and eggs in the feces. Neurocysticercosis can be confirmed through a CT scan, magnetic resonance imaging (MRI), and immunological tests (ELISA and RIA), while ophthalmoscopic examination helps to know about ocular cysticercosis.

6.6 Treatment

Oral administration of antthelmintics like praziquantel and niclosamide is effective against taeniasis in adults and children. Surgical removal of cysts is advisable in cases with intraventricular cysts causing obstruction, hydrocephalus, and ocular cysticercosis.

6.7 Prevention and control

• (i) Seeking medical help to treat tapeworm infestation in people. (ii) Prohibiting open defecation and promoting using toilets/latrines to avoid environmental contamination and infection of pigs and other people. (iii) Adopting good farming practices and preventing pigs from scavenging in contaminated areas. (iv) Vaccinating pigs/cattle and treating them simultaneously with appropriate antiparasitic drugs. (v) Inspecting meat to detect an infestation of parasitic cysts and discarding infected meat. (vi) Avoiding consumption of raw or undercooked pork. Always cook meat to at least 145–160° F (63–71°C) at its thickest part. (vii) Thorough cleaning of vegetables under running water and proper cooking. (viii) Promoting good hygiene practices such as washing hands with soap and water after using the toilets. (ix) Educating the people about the disease.

7. Toxoplasmosis

7.1 Etiology

Toxoplasmosis is caused by a hemoprotozoan parasite called Toxoplasma gondii.

7.2 Life cycle

Toxoplasma gondii has a complex life cycle; it reproduces asexually and sexually [56]. Cats and other felids are the only definitive hosts, while other mammals, including man and birds, are intermediate hosts. The sexual cycle of the parasite takes place in the intestinal epithelium of the definitive host, while the asexual cycle occurs in both the definitive and intermediate hosts [57].

7.2.1 Enteroepithelial cycle

Cats acquire the infection by consuming tissue cysts in chronically infected intermediate hosts or ingesting oocysts in food or water. After ingestion of tissue cysts, the cyst wall is digested by gastric juices resulting in the release of bradyzoites. Bradyzoites invade the intestinal epithelium to convert it into an actively multiplying tachyzoite stage. Some tachyzoites undergo five different developmental stages inside the epithelium to reproduce asexually by endodyogeny. Two daughter cells are created, which undergo schizogony to differentiate into micro- and macrogametocytes within two days of infection. The gametes fuse to form a zygote, which subsequently secretes a cyst wall to develop into oocysts. Oocysts rupture the intestinal epithelial cells and are excreted in feces. Oocysts undergo sporulation outside the host’s body to become infective for other hosts. Cats with toxoplasmosis typically show no signs of the disease. The shortest prepatent period (PP), i.e., the time from infection until the shedding of oocysts, is 3 to 10 days after ingestion of tissue cysts. In contrast, it is 13 days or more after consuming tachyzoites and 18 days or more after oocyst ingestion [57]. Almost all cats shed oocysts after tissue cysts’ ingestion, whereas less than 30–50% of cats shed oocysts after ingesting tachyzoites or oocysts [58].

7.2.2 Extraintestinal cycle

When the intermediate host ingests oocysts, sporozoites are released into the gut lumen and pass through the gut epithelium to enter cells in the lamina propria. If the intermediate host ingests tissue cysts, the released bradyzoites behave like sporozoites. Both sporozoites and bradyzoites transform into tachyzoites that enter a host cell, dividing rapidly until the cell bursts. Tachyzoites continue to invade adjacent cells or travel elsewhere in the body through the bloodstream. As the host’s immunity develops, the replication of tachyzoites decreases, resulting in the conversion of tachyzoites into a slowly dividing bradyzoite (tissue cysts) which do not typically produce a host reaction. The parasite’s life cycle is completed when felidae ingests the flesh of an intermediate host containing tissue cysts.

7.3 Epidemiology

The prevalence of T. gondii varies in different geographical areas and among different ethnic groups, with warm and humid climates being more conducive to its spread [59, 60]. T. gondii infections are widespread and estimated to affect up to one-third of the world’s human population [59]. The disease has been documented in numerous countries globally [60, 61]. The prevalence of latent toxoplasmosis in pregnant women globally is 33.8%, with the highest prevalence in South America and the lowest in the Western Pacific region [62]. Developed countries such as France have seen a decrease in Toxoplasma infection rates due to changes in food habits and hygiene measures [63, 64]. Toxoplasmosis causes reproductive disorders in various hosts, resulting in economic losses to the sheep industry worldwide [58, 61]. Goats are highly susceptible to clinical toxoplasmosis, while pigs are unaffected.

7.4 Transmission

High temperature and humidity favor the survival of T. gondii oocysts in the environment. Rodents are considered reservoir hosts, significantly transmitting the disease to domestic animals and humans. Cats are a crucial part of the transmission cycle of T. gondii, as they are the only species capable of shedding oocysts in their feces. The congenital transmission from an infected mother to her child has been reported in humans during pregnancy. Human infection can also result from ingesting food or water contaminated with oocysts [65] and consuming raw or undercooked meat containing tissue cysts. Infection can also be transmitted by transfusion of blood or tissues from infected animals harboring tachyzoites or bradyzoites.

7.5 Disease

7.5.1 Disease in man

• Congenital toxoplasmosis: If the mother has a primary infection or is a carrier of a chronic infection, the cysts can infect the fetus during late pregnancy. The mother may not experience symptoms. Severe cases can result in abortion, while surviving fetuses may exhibit symptoms such as fever, enlarged spleen and liver, and developmental delays. Delayed manifestations of toxoplasmosis in children include cataracts, eye inflammation, anemia, and mental retardation.

• Acquired toxoplasmosis: In 25% of cases, the disease produces no noticeable symptoms. However, the disease can be severe in people with weakened immune systems. Symptoms may range from fever and body pain to life-threatening encephalitis. Common manifestations of the disease include fever, swollen lymph nodes, high levels of lymphocytes in the blood, unexplained eye lesions, pregnancy complications, heart inflammation, and brain inflammation.

7.5.2 Toxoplasmosis in animals

Toxoplasma gondii can infect cattle, sheep, goats, pigs, dogs, and horses. Symptoms may include respiratory, enteric, and nervous system issues and fevers. Abortion and congenital transmission only occur in sheep.

7.6 Diagnosis in man and animals

Isolation of parasite is carried out by inoculating laboratory mice with fetal brain and placental cotyledons. Several serological tests are available for the detection of T. gondiiantibodies, including the Feldman dye test, indirect hemagglutination test, complement fixation test, modified agglutination test, latex agglutination test, direct agglutination test, indirect fluorescent antibody test, and enzyme-linked immunosorbent assay.

7.7 Treatment

There is no effective treatment or prophylaxis for farm animals. However, sulfonamides, pyrimethamine, and clindamycin can be therapeutic in dogs and cats.

7.8 Prevention and control

Proper biosecurity measures should be implemented at farms. Aborted materials and contaminated water should be discarded immediately to avoid consumption by domestic or feral cats. Pet cats should be kept indoors to prevent them from hunting infected rodents. Avoid feeding raw/undercooked meat to cats. Vaccination of cats should be done. An infection can be prevented in sheep by vaccinating with the live-attenuated tachyzoite S48 strain vaccine, licensed for sheep in New Zealand, the UK, Ireland, and France. Infection in humans can be prevented by adequate cooking and thorough meat freezing. Pregnant women should avoid direct and indirect contact with cats. Education for health professionals and people, in general, is also necessary.

8. Trichinellosis

8.1 Etiology

Trichinellosis or trichinosis is caused by a roundworm (nematode) called “Trichinella.” There are nine species and 12 genotypes of Trichinella. T. spiralis is the most common species causing human disease. However, other species, such as T. pseudospiralis, T. nativa, T. murelli, T. nelsoni, T. britovi, Trisinuata papuae, and T. zimbabwensis, are also implicated in human infection.

8.2 Epidemiology and transmission

Human trichinellosis is mainly linked to the consumption of infected pork, often reported in Central and South America, Asia, and Europe [66]. Domestic pork and related products are the critical sources of Trichinella infection in humans, primarily obtained from pigs raised under free-ranging practices [67]. Raw horse and dog meat consumption in countries like France and China has led to Trichinella outbreaks [68, 69]. Hunters risk infection when consuming raw meat from game animals [70]. Illegal importation of uncontrolled meat from endemic to non-endemic countries resulted in outbreaks in Denmark, Germany, Italy, Spain, and the United Kingdom [71, 72, 73]. In countries such as Israel, Lebanon, and Syria, where pork consumption is forbidden by the Judaic and Muslim religions, outbreaks of trichinellosis have only been observed in specific populations who consumed pork from wild boars [74, 75].

8.3 Life cycle

Adult worms and larvae develop within a single vertebrate host, which can serve as both a definitive and an intermediate host. In order to complete its life cycle, Trichinella requires a second host. In the domestic life cycle of the parasite, pigs and rodents are frequently involved. In sylvatic cycles, wild animals, such as bears, moose, and wild boars, are the primary reservoirs. In the initial stage of trichinellosis, Trichinella larvae are present in the muscle of hosts. When a new host ingests infected muscle tissue, larvae are released during digestion, enter the small intestine, and move to the jejunum and ileum to mature into adult roundworms. A single adult female worm produces around 1500 newborn larvae. The larvae leave the intestine and enter the blood circulation to reach muscle tissues, where they mature and become coiled within the muscle fibers. In some cases, larvae are encapsulated due to the host’s cellular response and form a host–parasite complex called the nurse cell. The larvae can survive within the nurse cell for months or years, receiving nutrients and oxygen from an increased vascular supply. Eventually, the encapsulated cyst becomes calcified, leading to the death of the larva. It takes 17 to 21 days from exposure to the appearance and encystment of larvae in muscles. Infected animals are partially immune to subsequent infections due to intense and persistent immunity.

8.4 Disease

Disease symptoms depend on the infecting dose, the individual’s susceptibility, and the species of Trichinella involved. The disease’s initial phase is known as the “enteral phase,” which appears as early as 1 week after ingesting the infective dose. It is characterized by abdominal discomfort and diarrhea lasting a few days. The parenteral phase of the disease may occur within 1 to 2 weeks following infection, or it may be delayed for several weeks as more significant numbers of worms migrate and accumulate in the musculature. Symptoms of the parenteral phase include periorbital edema, myalgia, headache, fever, macro-papular rash, and conjunctival and subungual hemorrhages. Complications of trichinellosis may lead to myocarditis and encephalitis due to migration of larvae to the heart musculature or the central nervous system.

8.5 Diagnosis

The compression method is the oldest and the most common direct detection method for Trichinella larvae in meat samples. A minimum of 1 gram of tissue must be examined to achieve a theoretical sensitivity of 1 larva per gram, which is considered the threshold for infection to pose a public health risk. The magnetic stirrer method is the “gold standard” for detecting Trichinella larvae in pooled samples [76]. ELISA can test animals for anti-Trichinella antibodies in their serum or meat juice (10⁸) due to its high sensitivity for detecting as little as one larva per 100 grams of muscle tissue [77]. The most commonly infected animal muscle tissues are the diaphragm crus, tongue, and masseter muscle [76].

8.6 Treatment

The recommended dosage for albendazole is 400 mg twice daily for 8 to 14 days or mebendazole (200 to 400 mg) thrice a day for 3 days, followed by 400 to 500 mg three times a day for 10 days. Both treatments are suitable for adults and children but are not advocated for pregnant women or children under the age of 2 years [78]. In pregnant women and children, a single dose of pyrantel (10 to 20 mg/kg body weight) for 2 to 3 days is effective against worms in the gut but does not affect newborns and muscle larvae [79]. Prednisone (30 to 60 mg/day) for 10 to 15 days is a standard chemotherapy choice for severe symptoms.

8.7 Prevention and control

Trichinellosis is a 100% foodborne parasitic disease that can be prevented by thoroughly cooking meat to an internal temperature of 71°C (160°F) or higher. Freezing meat at −15°C (5°F) for at least 3 weeks can also kill Trichinella larvae. Additionally, avoiding consuming raw or undercooked wild game meat, especially pork, can reduce the risk of infection. In some countries, mandatory inspection and testing of pork products have controlled the incidences of trichinellosis.

9. Conclusion

Neglected zoonotic diseases mainly affect existing populations of low socioeconomic status residing in urban slums and villages and those engaged in poor animal husbandry practices. According to disability-adjusted life years (DALYs) tracked by WHO, OIE, 6 out of 20 infectious zoonotic diseases are neglected. NTDs globally affect more than 1.4 billion people, mainly poor and marginalized populations in low-resource settings. Understanding NTDs is essential to reduce human health risks by controlling animal infections. The primary concern with NTDs is the critical gap between public health needs and veterinary responsibilities, the paucity of research grants for NTDs, the negligence of policymakers, limited diagnostic capacity, and the need for coordinated control and prevention programs.

Conflict of interest

The authors declare no conflict of interest.