There are many important species of coccidia that effect many animals especially mammals and birds. The most common genera are Eimeria and Isospora. The life cycle of these parasites involves the ingestion of sporulated oocysts (above, left) containing sporozoites. Sporozoites penetrate intestinal cells, feed, grow and eventually go through a-sexual reproduction called schizogony. The end result of this division is the production of merozoites which rupture from the infected cell and enter new cells. At some point, some merozoites begin the sexual phase of the life cycle, being micro and macro-gametes. Fertilization occurs and a zygote is produced within the host cells. The zygote is called a oocyst and eventually passes out of the intestine with the feces in an unsporulated form (above, right). In all instances, the number of asexual cycles is pre-determined. Pathogenesis is related to intestinal cell distruction. Fever is not common unless secondary infection occurs. Bloody diarrhea is common in some infections with a resulting anemia. In general, the disease caused by coccidia varies not only with the state of the host, but with the species of coccidia, the degree of parasitism, and the site of infection. In addition to clinical signs associated withthe intestinalcell distruction, vague related signs may olso occur such as rough hair coat, poor weight gains or weight loss, and emaciation. In severly infected animals, death may occur and inothers, central nervous system disorders may be notable.
Diagnosis is dependent on microscopic detection of oocysts in feces or by identification of endogenous stages obtained by scrapings of intestinal cells.
Treatment usually involves sulfonamides, nitrofurazone, or amprolium. Amprolium appears to be both cocciciostatic and coccidiocidal.
Cryptosporidium spp - This parasite is similar to most coccidia except that the organism is not considered to be host specific and is located in parasitophorous vacuoles just under the surface membrane of host cells or within its striated border rather than within host cells. Additionally, the oocysts are small in size (4-6 micrometers), and sporulation can occur internally resulting in sporulated oocysts being passed in the feces, Some species are thought to be host specific while others are easily transmitted among diffrent species of animals. Transmission is by the fecal-oral route.
There are many species of Cryptosporidium capable of infecting many animals. Clinical cryptosporidial infections in calves are characterized by diarrhea often occuring around the second week of life. Appetite usually remains good and dehydration is minimal in uncomplicated cases. Stools often have a rancid odor, a yellow to white color and are putty-like in consistency. Cryptosporidia infections are among the four most common pathogens associated with neonatal diarrhea in calves. It is common in both beef and dairy calves as well as lambs. The organism appears to have a worldwide distribution. Zoonotic infections in humans are common. In most cases, diarrhea is the clinical problem resulting from infection. Natural self-limiting infections are the rule in immunocompetent animals. Cats, dogs, calves and many young ruminants may become infected and develop a fulminating diarrhea. Gross pathologic lesions in the small intestine are not common although histologic evaluation may reveal atrophy of the villi in the small intestine. There is no effective drug for the treatment of cryptosporidiosis. Antibiotics are often contraindicated and treatment should consist of supportive therapy.
Diagnosis is by microscopic detection of sporulated oocysts in feces or by histologic examination of intestinal tissue. A presumptive diagnosis can be made based on the age of the animal and the nature of the clinical signs.
Additional Link:
Cryptosporidium Research at Kansas State
Portions of the Toxoplasma life cycle are similar to that of the typical coccidia. This phase occurs in the intestine of felines. Additional portions of the life cycle occur in rodents, rabbits and birds.
The enteroepithelial (coccidia-like) life cycle in felines is initiated when cats ingest intermediate hosts infected with tissue cysts. Bradyzoites are released from the cysts in the feline stomach and penetrate the epithelial cell of the small intestine. This is equivalent to schizonts in other intestinal coccidia infections. Oocysts are eventually produced from gamete fertilization and are passed in the feces. Oocysts are unsporulated when passed. The entire coccidian life cycle takes about 3 days to complete after infection.
Extraintestinal development of T. gondii is the same in all hosts and is not dependent upon whether tissue cysts or oocysts are ingested. After sporulated oocysts are ingested, sporozoites are released and they penetrate intestinal cells becoming tachyzoites. These multiply in almost any cell in the body. Infected cells either rupture releasing tachyzoites or encyst resulting in bradyzoites. Bradyzoites are similar to tachyzoites except that they can survive the digestive process while tachyzoites can not. These cysts are found in the CNS, muscles, visceral organs and may persist for the life of the host. Cysts are not lobulate or septate.
Congenital infection can occur if infection occurs during pregnancy resulting from placentitis followed by spread of tachyzoites to the fetus.
Clinically, feline toxoplasmosis is most severe in transplacentally infected kittens. Affected kittens may be stillborn or die before weaning. Clinical signs reflect inflammation of the liver, lungs and CNS. Clinical signs of postnatal toxoplasmosis include anorexia, lethargy and dyspnea owing to pneumonia.
Clinical signs in dogs may be localized in respiratory, neuromuscular, or gastrointestinal systems or may be generalized. The neurological form may last for several weeks without involving other systems while disease of the lungs and liver may result in death within a week. Generalized toxoplasmosis in the dog is most common in dogs under 1 year of age. The most dramatic clinical signs in older dogs are associated with the neural and muscular systems. Seizures, cranial nerve deficits, tremors, ataxia and paralysis are all reported. Ocular lesions are also reported.
Diagnosis is determined by the phase of infection, the host involved, and availability of testing. Hematologic and biochemical parameters are of value in acute cases in both the dog and cat. Tachyzoites (above) can be recovered and detected microscopically or through culture and/or animal inoculation from a variety of body fluids. Radiographic findings, especially in the cute phase, consist of a diffuse interstitial to alveolar pattern with a mottled lobar distribution. Fecal examination of felines is of little value since cats usually shed T. gondii oocysts for only a few weeks after their first exposure. Serologic testing is useful with new tests that detect changes in immunoglobulin classes becoming available.
A similar tissue cyst-forming organism , Neospora spp has been reported from canines and bovines causing myocarditis, encephalitis and myosistis. Morphologically, the organism resembles Toxoplasma except that some of the cysts have thick walls. Antigenic and ultrastructural studies have indicated Neospora to be a distinct species.
Treatment with Clindamycin is usually effective in surpressing replication of the parasite but does not completely kill the parasite.
Remember, toxoplasmosis is a zoonotic disease and of public health concern. There are three infective stages (sporozoites, tachyzoites and bradyzoites) and human exposure to them should be minimized.
The life cycle of this parasite is similar to that of Toxoplasma except common host is canines instead of felines. Infections are ubiquitous in reptiles, birds and warm-blooded mammals. Most cattle and sheep are infected. The life cycle is an obligatory two-host cycle with carnivores serving as the definitive host. Sarcocystis forms tissue cysts in muscle (above) and neural tissue of the intermediate hosts. The life cycle differs from most coccidia in that the oocysts are sporulated when passed in the feces. Intermediate hosts become infected by eating oocysts or sporocysts. Several generations of schizogony occur in blood vessels or hepatocytes (depending on the host) and merozoites invade muscle and nerve cells. Cysts posess septa.
There are many species of Sarcocystis that infect dogs and cats but none are pathogenic. As a result , no treatment is necessary but infection can be prevented by feeding only cooked meat.
Many wild animals including deer and elk are infected with the tissue stage of Sarcocystis. Completely cooked meat renders these stages harmless.
Sarcocystis falcatula is the causative agent for Equine Protozoal Myeloencephalitis (EPM). This disease has been reported from a number of states and provinces in horses ranging from two months to 19 years of age. Most cases effect animals four years of age or younger. Like all members of this genus, the life cycle involves an intestinal coccidia-like cycle in carnivores in which the infective oocysts (containing sporozoites) are shed in the feces. In this case the definitive host is thought to be the opossum. Infection of the intermediate host (equine) occurs from ingestion of ocysts contaminated feed and water. Problems arise in the horse infected with this parasite when the merozoites pass through the vascular endothelium of the blood-brain barrier and reach the CNS. Pathogenesis is related to multifocal areas of hemorrhage of the brain and/or spinal cord. Inflammaton and necrosis is also common.
On presentation, infected horses will be alert and responsive. There is usually a gate deficit (ataxia) with signs of muscle atrophy. Horses are reluctant to move their rear legs from a supported position and have difficulty backing up. Diagnosis of EPM is often difficult. Increased protein levels in cerebral spinal fluid (CSF) and increased WBC levels are often seen. Serologic tests are becomming available to detect Sarcocystis antibody in CSF. However, histologic evaluation at necropsy is often the only positive means od fiagnosis.
Treatment involves trimethoprim sulfamethoxazole therapy at 15 mg/kg, per os. Additional therapy with pyrimethamine (0.25 mg/lb for 3 days followed by once a day for 27 days (per os)) is recommended. In severe cases, pyrimethamine has been given at higher dosages for 30 to 60 days. Success rates (suppression of the progress of clinical signs) in treated animals is 50 to 60%.
For more details on this parasite:
Hammondia
There are two species in domestic animals. H. hammondiin cats and H. heidorni in canines. Both are obligatory two-host parasites with life cycles similar to Toxoplasma. For H. hammondi goats and rats are intermediate hosts while humans and other mammals are intermediate hosts for H. hammondi. The generalized life cycle involves the intermediate hosts becoming infected by eating sporulated oocysts. Sporozoites excyst and invade intestinal cells, become tachyzoites and multiply. The parasite eventually encysts in muscles.
Frankelia microti. This tissue-cyst forming coccidian parasite is similar to Sarcocystus. The brain cysts are lobulate and contain septa.
Besnoitia spp.
This parasite has a life cycle that is similar to Hammondia with intermediate hosts (rodents, opossums and lizards) becoming infected by ingesting sporulated oocysts while cats are infected by ingesting tissue cysts. Schizonts and gamonts are formed in intestinal cells and the resulting oocysts are shed in the feces. The clinical manifestations are sub -cutanious (above left) or cutanious, often referred to as "elephant skin". Many believe that the organism may be mechanically transmitted by biting arthropods.
Cats but not dogs are definitive hosts for Besnoitia spp found in the U.S.
In Africa, bovine besnoitiosis is widespread but has been reported as well in France, Portugal, Isreal, Kazakhstan, south Korea and Venezuela. Besnoitia besnoiti is the causative agent and although feline hosts are known for some species, in B. besnoiti infections transmission has only been documented by mechanical transmission of bradyzoites. The bradyzoites are introduced on the mouthparts of biting flies and enter the circulation and multiply in endothelial cells of blood vessels in the superficial tissues. Resulting cells (tachyzoites) are released from endothelial cells and re-invade other endothelial cells. The result is vasculitis, increased permeability of vessels and anasarca. This initial stage is refered to as the anasarca stage.
Cyst formation occurs in the endothelium. Connective tissu reactions around the cysts produce a thinkening of the skin and resulting circulation disturbances, alopecia and necrosis. This stage is refered to as the scleroderma stage.
The disease in South Africa can be mild or severe but usually non-fatal. Most bovines do not show overt clinical signs with a few cysts on the scleral conjunctiva being the only indication of infection. The disease is of economic importance, however, since bulls fron non-endemic areas brought into endemic areas often become sterile after infection and slaughter carcasses are generally condemmed for human consumption.
Presently, there is not an effective treatment but a newly developed vaccine derived from a viscerotropic strain of Besnoitia found in wild blue wildebeest has been successful in preventing clinical forms of the disease
Histologic sections reveal numerous organisms (bradyzoites) in cutanious tissue (above right).
Hepatozoon spp-
Members of this genus are parasites found in white blood cells of a variety of animals. Transmission of H. canis involves the brown dog tick. (Rhipicephalus sanguineus) which transmits the infection to dogs when the infected tick is ingested. Both nymphal and adult ticks can transmit the infection.
Most dogs that are naturally infected with H canis do not develop clinical signs unless concurrently infected, immunosuppressed, have a defective neutrophil function, or are younger than 4 months of age.
Recently, a new species, H. americanum has been described from North America. This species differs from H. canis in that gamonts in leukocytes are rare, muscle stages are common, and periosteal bone proliferation is common. The entire life cycle and the vector(s) are still under investigation.
Other clinical signs include muscular hyperesthesia with lumbar pain, reluctance to move, gait abnormalities, oculonasal discharges, diarrhea, anorexia, fever, and weight loss. H. americanum has been reported from both domestic and wild canids. Non-clinical casesare also reported in wild and domestic felids
Diagnosis is by identification of gametocytes in leucocytes in peripheral blood films (above) or by radiographic detection. Radiographic findings may be nonexistent or spectacular. Microscopic detection of tissue stages in muscle appears to be the most consistant means of diagnosis. Most cases in domestic canines have previously occured in south-Texas although recent reportings in Georgia, Tennessee, Florida, Mississippi and Oklahoma indicate an expanding distribution for this parasite.
No treatment is proven effective in eliminating the organism but palliative treatment with nonsteroidal anti-inflammatory drugs appear to be helpful in relieving discomfort and may provide temporary clinical relief.
Haemogregarines
Parasites belonging to the genus Haemogregarina infect turtles and other reptiles, some amphibia and fish. The life cycle for most species of haemogregarines are unknown although leaches are assumed to be the vector for some aquatic vertebrates. Gametocytes present in amphibian, reptile or fish blood or plasma appear to exist without causing any ill effects. Clinical signs of anemia or thrombocytopenia have been reported in overwhelming infections. No known chemotherapeutic agents are known to be effective although chloroquin phosphate and primoquin phosphate used in combination has been proposed.
Additional genera including Karyolysus, Schellakia, Pirhemocyton Sauroplasma, Chelonplasma, and Serpentoplasma have been identified as intracytoplasmic parasites of reptile erythrocytes, their exact taxonomic positon(s) (and perhaps even their existance) is not uniformally agreed upon.
Encephalitozoon (Nosema) cuniculi.
This is a intracellular microsporidian parasite found in cytoplasmic vacuoles of renal tubular epithelial cells, endothelial cells, tissue macrophages and hepatocytes. Once thought to be similar to Toxoplasma, it is now recognized that members of this genus lack an apical complex and posess microsporidian polar tubes and capsules. Natural infections are reported from domestic and wild canines, rodents, felines, and other wild carnivores. Although the life cycle in nature is not totally known, canine encephalitozoonosis is a kennel problem when large numbers of animals are confined under less than desirable sanitary conditions.
Clinical signs depend on the time, course, and location of tissue damage. In neonates, clinical signs appear a few weeks postpartum, showing stunted growth and unthriftiness. As the course of infection progresses, animals show renal failure and neurologic signs such as depression, ataxia, convulsions and blindness. Animals may develop signs of aggressive behavior.
Clinical signs in cats vary from asymptomatic to severe muscle spasms, depression, paralysis and death.
Clinical laboratory findings are non-specific being usually a normochromic, normocytic anemia consistent with severe renal lesions with depression of erythropietin production. Hematuria and pyuria may be present on urinalysis.
Diagnosis is dependent on finding spores, usually shed in the urine from parasitized renal tubular epithelial cells. Spores are identifiable microscopically in the urine sediment with Gram or Ziehl-Neelsen staining. Positive identification requires immunochemical testing procedures to separate this parasite from coccidia and Toxoplasma. Serologic detection of antibody (IFA and ELISA) are useful but cross react with other microsporidia.