**3. Epidemiology**

#### **3.1 Dogs and cats**

*T. canis* is the most common nematode in dogs in many regions of the world and *T. cati* in cats. In a meta-analysis study where data from more than 13 million dogs from 60 countries were included, the overall prevalence of *Toxocara* infection in dogs was found to be 11.1%. The prevalence was estimated in different World Health Organization regions: Eastern Mediterranean (19.2%), Africa (18.5%), South-East Asia (11.9%), North America (11.1%), South America (10.9%), Europe (10.8%) and Western Pacific (6.4%) [7].

In a second meta-analysis where data from 2,158,069 cats from 51 countries were included, an overall prevalence of *T. cati* of 17% was found. The prevalence was estimated in different World regions: African (43.3%), Eastern Mediterranean (21.6%), North America (18.3%), Europe (17.8%), Western Pacific (17.3%), South-East Asia (14.9%),and South American (12.6%)[8].

Transplacental transmission from bitches to their puppies is the most important form of *T. canis* infection in dogs. Not all somatic larvae in bitches are reactivated during the same gestation; thus, reactivation of larvae occurs in subsequent gestations. In addition, bitches become reinfected by ingesting persistent larvated eggs in an environment contaminated with fecal matter from their puppies. Transplacental transmission does not appear to occur in cats with *T. cati*, making lactogenic infection the most common form of infection in kittens [4, 6].

Puppies are the main source of environmental contamination; they can excrete eggs in feces from 15 days of birth, and the greatest egg shedding occurs between 1 and 3 months of age, when they can eliminate more than a million eggs per day. Gradually, the worm burden in the intestine tends to decrease, and they stop shedding eggs before reaching 6 months of age. In addition, the larvae ingested by the lactogenic route gradually increase the worm burden and the elimination of eggs in the puppies. Puppies under three months of age are the only hosts that can develop adult worms in the intestine by ingesting larvated eggs, although apparently, this is not their main route of infection [9].

Adult *Toxocara* females are very prolific, producing between 25,000 and 85,000 eggs per day, and the presence of many females in the intestine of a puppy can mean the elimination of enormous numbers of eggs in the feces (>100,000/g). In the environment, when eggs are protected from direct sunlight and desiccation, they develop to the infective stage (L3 passive) 2–4 weeks after shedding. In earthen soils, the eggs can remain viable for many months, accumulating in the environment. Therefore, the soil in areas where dogs with toxocariosis commonly defecate is considered a permanent source of infection for animals and humans. In addition, rainwater can carry the eggs to distant places and accumulate them in large concentrations in some places [1]. A study that included 42,797 soil samples in 40 countries showed a global prevalence of *Toxocara* eggs in public places of 21%. The estimated prevalence rates in the different regions ranged from Western Pacific (35%), Africa (27%), South America (25%), South-East Asia (21%), the Middle East and North Africa (18%), Europe (18%) and the North and Central Americas (13%) [10].

Paratenic hosts infected by ingesting larvated eggs present in soil, food or water accumulate L3 in their tissues. If these are predated, they can be a source of infection for adult dogs. If predated by another paratenic host, the larvae can infect the new host, bypassing a definitive host.

#### **3.2 Humans**

Due to the great difficulty of identifying the physical presence of somatic larvae, the most common way to identify *Toxocara* infection in humans is by serological tests (ELISA and Western blot). Serologically, it is not possible to distinguish between a *T. canis* infection and a *T. cati* infection, and although *T. canis* infection has generally been considered to be the predominant infection in humans, the seroprevalence of *T. cati* has not been determined, which could have been underestimated [11].

The seroprevalence of *Toxocara* in humans varies in different regions of the world. A meta-analysis carried out in 2019 that included 265,327 participants in 71 countries showed an estimated global *Toxocara* seroprevalence rate of 19.0%. The pooled seroprevalence for regions was as follows: African (37.7%), South-East Asia (34.1%), Western Pacific (24.2%), American regions (22.8%), European regions (10.5%), and Eastern Mediterranean region (8.2%) [12]. Seroprevalence has been associated with different risk factors, such as age, contact with young dogs and kittens, socioeconomic level, consumption of vegetables, and unboiled water, ethnicity, educational level, living in a rural area and pet ownership [13, 14]. The serological differences associated with the different ethnic groups in some countries may be the result of different contextual exposures linked, among other factors, to their socioeconomic level, segregation, and the environmental conditions in which the different ethnic groups live, and not necessarily due to a genetic predisposition [15].

The most common way of infection in humans occurs through the accidental ingestion of *Toxocara* larvated eggs, which can be found on soil in public parks, gardens, dirt floors, sandboxes, and vegetables irrigated with sewage, among others. Although people of any age can be infected, children are more frequently affected due to their habits of playing with pets and dirt, geophagia, and pica, in addition to their commonly poor hygiene habits [16–18]. Infection can also occur through the ingestion of somatic larvae present in raw or undercooked meat and viscera of cattle, pigs, and poultry, among others, which act as paratenic hosts (**Figure 1**) [19–22]. *Blattella germanica* and *Periplaneta americana* cockroaches have recently been shown to be able to ingest and shed larvated *T. canis* eggs in their feces, suggesting that they could carry infective eggs from dog feces to kitchens where human food is prepared [2].

There are multiple reports of the presence of *Toxocara* eggs in the hair of dogs and cats, which is why it has been proposed that they are a source of infection for their

*Toxocariosis: From a One Health Perspective DOI: http://dx.doi.org/10.5772/intechopen.104508*

#### **Figure 1.**

*Epidemiology of toxocariosis from the one health approach. The biological cycle of* Toxocara *sp. involves definitive (dogs and cats), paratenic (several species of mammals and birds), and incidental (human) hosts. Puppies are the main eliminators of immature eggs into the environment (1). In optimal environmental conditions of humidity and temperature, passive larvae 3 develop inside the eggs, which are the main infective stage for all hosts (2). Paratenic or incidental hosts that ingest larvated eggs maintain somatic larvae in their tissues (3) that are infective to predators of the infected paratenic host. Human infection occurs mainly by ingestion of larvated eggs or by ingestion of raw animal meat or viscera (chicken, pig, beef) with infective somatic larvae (4). The ingestion of larvated eggs can be facilitated by the consumption of contaminated vegetables (5). Somatic larvae present in the definitive host are transmitted to puppies by transplacental (dog) and lactogenic (dog and cat) routes (6). Blue arrows show the dynamics of egg development in the environment, red arrows show transmission from larvated eggs, and yellow arrows show transmission from somatic larvae.*

owners [23–26]. However, the presence of larvated infective eggs in the hair is very low, probably due to poor temperature and humidity conditions [27], suggesting a low risk of infection for humans when petting the hair of their pets, although the possibility exists.

### **4. Canine and feline toxocariosis**

#### **4.1 Pathogenesis and clinical picture**

The adult worms of *T. canis* and *T. cati* feed on intestinal content, compete with the host for nutrients and, depending on the worm burden, can produce different

degrees of malnutrition. The presence of adult worms causes intestinal irritation, which induces decreased absorption of nutrients and is responsible for diarrhea and vomiting observed in some young animals. The presence of adult worms in the intestinal lumen exerts a mechanical obstructive action on the normal flow of intestinal content. Microscopically, the presence of adult worms produces mucosal muscular hypertrophy, intestinal villus atrophy, and crypt hyperplasia [1].

Larval migration in mild or moderate infections in puppies generally does not produce obvious clinical signs; however, larval migration in severe infections produces respiratory signs such as tachypnea, cough, and runny nose. Nervous signs such as incoordination or convulsions are occasionally observed in puppies due to the passage of the larvae through the brain. In puppies with intense prenatal infection, the lesions produced by the passage of the larvae in the liver, lungs, or central nervous system can cause the death of the puppies in the first 2 weeks of life [28].

Mild to moderate adult worm infections in puppies are usually asymptomatic or cause mild digestive symptoms and growth retardation. In severe infections, dirtylooking bristly hair, rough skin, painful intestinal distention, vomiting (frequently with adult worms), bulging abdomen (mainly when they have just eaten), presence of large amounts of gas produced by intestinal dysbiosis, alternating periods of constipation and diarrhea with profuse mucus, decreased appetite and growth retardation, can be observed. The blood count shows eosinophilia and anemia. Occasionally, there may be the death of puppies due to aspiration of vomit and intestinal obstruction or rupture. The presence of large numbers of adult worms as a result of massive prenatal infections in puppies can cause complete obstruction of the intestinal lumen, intussusception of the small intestine, and death of the entire litter [9, 29, 30].

In kittens, there is no transplacental transmission; therefore, the development of adult worms occurs until almost 30 days of age and the beginning of the elimination of eggs at approximately 50 days of age. The clinical picture is similar to that described in dogs but less severe, diarrhea, vomiting, and loss of appetite predominate, and deaths are very rare. The highest incidence of *T. cati* in cats occurs between 2 and 6 months of age; in general, the worm burden is lower in kittens than in puppies and occurs when the kittens are older and therefore have a higher degree of development [9, 31].

#### **4.2 Diagnosis of toxocariosis in dogs and cats**

Sporadically, shed adult worms can be observed macroscopically in the vomit or feces of puppies. The detection of *Toxocara* eggs in feces is performed by coproparasitoscopic techniques, such as Faust or McMaster; however, this can only be done when there are adult stages in the intestine, mainly in puppies [3]. In the eggs, three external layers are observed, forming the shell; the outermost layer is albuminous, the middle layer is lipoid, and the inner layer chitinous. The shell has depressions on the surface, called pits, which give it an appearance similar to a golf ball. The egg measures 75–85 μm and has a protoplasmic mass that occupies the entire interior.

In adult dogs and paratenic hosts, infection by somatic larvae can be demonstrated by the detection of specific antibodies against excretion-secretion antigens using immunological techniques such as ELISA or Western blot; however, due to their cost, difficulty in obtaining the antigens, and their difficult implementation, these techniques are not widely used in the veterinary field [32].
