Chapter 5

PHYLUM APICOMPLEXA

 

 

 

5.1 GENERAL COMMENTS

5.1.1 Classification

 

 

5.1.2 Members of the phylum Apicomplexa

A. Coccidia and related organisms

* Though recently researchers have broadened the term to include other genera, we will restrict our use of the term coccidia to its classical referral to the Eimeria and Isospora.

B. Malaria and malaria-like organisms

C. Piroplasms

5.2 COCCIDIAL PARASITES

Coccidia in the genera Cryptosporidium, Eimeria, Isospora, arcocystis, and Toxoplasma are the most economically important group of protozoans in domestic animals in the United States. Historically the structure of the sporulated oocyst, especially the number of sporocysts and sporozoites, was used as a major characteristic to differentiate genera of coccidia.

Figure 2.25 provides a comparative guide to the morphology of sporulated oocysts among these and other genera of coccidia. This figure is a stylized illustration of sporulated oocysts representative of coccidian genera. Below each oocyst is the name of a genus in which that morphologic form is found. Above each oocyst is the number of sporocysts and sporozoites found in each oocyst of that genus. 

 

Figure 2.25: Sporulated Oocysts representative of Coccidian genera 
 

5.2.1 EIMERIA AND ISOSPORA
 

G. Detailed Life Cycle of The Coccida Eimeria and Isospora

Infection of the definitive host begins with the ingestion of infective oocysts containing fully developed sporozoites (within sporocysts) which are freed in the lumen of the intestine by enzymic action of digestion upon the oocyst wall. The freed motile sporozoites penetrate epithelial cells of the intestine and round-up to form trophozoites which undergo a form of internal budding or cell division which is termed a schizont at this point (or schizogony the process). The later process (first generation schizonts) is terminated when the round internal cells elongate or become sickle shaped (which are termed merozoites, first generation) and are released (rupture host cells) into the intestinal lumen to enter other cells in their vicinity and repeating a second and/maybe a third generation of schiogony (merogony). Most merozoites of the second generation form macrogamethocytes with macrogametes which undergo no cell division. Those merozoites which develop into microgametocytes undergo further division forming biflagellated microgametes. The later leave host cells to penetrate other cells containing macrogametes resulting in fertilization, forming the zygote. The latter lays down a wall around itself from the eosinophilic plastic granules in its cytoplasm, thus forming the oocysts which breaks out of the host cells to be passed in the feces to sporulate or become infective in about 2-3 days under ideal conditions of temperature (Sporogony).

 

Figure 2.27: Life Cycle of Eimeria

 

Figure 2.28: Detailed Illustration of the Life Cycle of Eimeria  
 

 

 

Figure 2.29: Life cycles of Eimeria and Isospora

5.2.2 TOXOPLASMA GONDII

5.2.2.1 Classification

5.2.2.2 Geographagic Distribution: worldwide

5.2.2.3 Epidemiology and Hosts

Toxoplasma is transmitted to cats that ingest either sporulated oocysts or tissues infected with tachyzoites, but the most common source of infection is ingestion of tissues containing cysts. On ingestion of cysts, bracyzoites released in the gastrointestinal tract initiate an enteroepithelial cycle of asexual and sexual multiplication, followed by oocyst development and shedding of unsporulated oocysts with feces. An extraintestinal cycle, like that seen in nonfelids, also occurs in cats.

5. Life cycle 

The coccidium Toxoplasma gondii infects all warm-blooded animals, including humans. Felids (both domestic and wild) are the only definitive hosts;

 

Figure 2.30: Life Cycle of Toxoplasma gondi

 felids and nonfelids are intermediate hosts. Toxoplasma can betransmitted to intermediate hosts via oocysts in feline feces, via cysts in host tissues (meat), and via techyzoites transplacentally. Unsporulated oocysts in feline feces sporulate outside the body and become infectious. On ingestion, sporozoites excyst and multiply in the intestine and associated lymph nodes as tachyzoites. Tachyzoites multiply by endodyogeny (see Figure 2.30) for numerous generations, spreading through tissues and circulation, and then encyst. Cysts persist most frequently in the brain, liver, muscles, and retina. They are usually spherical or elongate, thin-walled structures containing a few to several hundred slender PAS-positive bradyzoites or slowly multiplying zoites. Cysts ingested by a nonfeline host release bradyzoites, which become tachyzoitesm, and the cycle is repeated. Infection by either oocysts or cysts during pregnancy can result in transplacental infection of the fetus with tachyzoites.

 

Figure 2.31 Endodyogeny in Toxoplasma Gondii

 

Figure 2.32: Detailed life Cycle of Toxoplasma gondii in Feilds 

5.2.2.4 Pathology

Trachyzoite multiplication results in focal necrosis, the most characteristic lesion of toxoplasmosis. Inflammation usually follows necrosis. Pneumonitis is the predominant lesion in fatal toxoplasmosis in cats and dogs; placental necrosis with white flecks or multiple white, chalky, necrotic nodules and associated abortion predominate in sheep and goats. Histologcially, this necrosis is confined to the cotyledons where individual and small group of tachyzoites are often difficult to recognize among degenerating host cells. Encephalomyelitis is the predominant lesion in sheep. 

5.2.2.5 Diagnosis

Diagnosis of Toxoplasma is performed at postmortem by identification of organisms in infected tissue. Diagnosis in live animals is aided by serologic tests and by bioassay or xenodiagnosis in mice.

5.2.2.6 Prevention and Control

The following preventative measures apply to all persons, but because toxoplasmosis is most severe in the perintatal period, they should be emphasized for pregnant women and for young children.

The following preventative measures apply to farms and other animal-rearing facilities. Avoid contamination of feed or water with oocysts in cat feces by:

5.2.3 SARCOCYSTIS

5.2.3.1 Life cycle

Sarcocystis is a genus of cyst-forming coccidia with an obligatory two-host life cycle. cysts are found primarily in muscles of wild and domestic herbivores. Carnivores that prey on herbivore hosts become infected and serve as definitive hosts when zoites released by digestion of mature cysts invade the intestinal epithelium and develop directly into gamonts. Fertilization is followed by formation of oocysts, which sporulate within the intestine and are shed as infective oocysts or sporocysts in the feces of the carnivore.

On ingestion of oocysts or sporocysts by susceptible herbivorous mammals or birds, sporozoites are released (excyst) in the intestine. They migrate to arterial vessels where they develop into meronts. Merozoites liberated from these meronts initiate a second generation of meronts in capillaries throughout the body. Merozoites liberated from second generation meronts enter mononucleate cells found in the circulation and undergo endodyogeny within the cytoplasm of these cells. Merozoites from the circulation enter the heart and skeletal muscle cells and the neural tissue, where they develop into immature noninfective sarcocysts that contin unicellular metrocytes. Metrocytes produce bradyzoites that are infective for the predator animal and whos presence characterizes a mature sarcocyst. Sarcocysts of some species remain microscopic, whereas others become visible to the unaided eye.

5.2.3.2 Pathology

Some species of Sarcocystis are pathogenic to the herbivore intermediate host. Acute lesions characterized by hemorrhage, edema, and necrosis are associated with the maturation of second generation meronts. Macroscopic lesions observed postmortem may include generalized serous atrophy of fat, excessive yellowish fluid in all body cavities, watery blood, petechical hemorrhage in the heart and pericardium, serosa of the gastrointestinal tract and urinary bladder, edema and hemorrhage of lymph nodes, and alternate pale and dark striping or mottling of skeletal muscles. Microscopically, hemorrhage may be seen in all organs, and mononuclear cell infiltration into the perivascular tissues of the hear, skeletal muscles, lung, liver, and kidney may be mild to severe. Regenerative changes are most often associated with the myocardium. Chronic lesions charactgerized by muscle atrophy and myositis are associated with mature saccocysts. Specific macroscopic lesions may not always be seen postmortem. Microscopic lesions may include myositis and myocarditis. Most definitive hosts are clinically unaffected by Sarcocystis infection.

 

Figure 2.34: Life Cycle of Sarcocystis

 

Figure 2.35: Life Cycle of Sarcocystis

 

5.2.4 CRYTOSPORIDIUM

Coccidia of the genus Cryptosporidium are found in mammals, birds, fish, and reptiles. Historically, numerous species of Cryptosporidium were each thought to infect a single host species, but recent studies show that an isolate of Cryptosporidium from one mammlian host can infect several mammalian host species. Transmission is direct. Unusally small sporulated or unsporulated oocysts are shed in the feces. On ingestion or inhalation of sporulated oocysts, sporozoites are released and infect the epithelium in the digestive or respiratory tract.

Although asexual and sexual stages of Cryptosporidium are morphologically similar to those of other coccidia, they possess some unique distinguishing characteristics. All stages are small and are located at the microvillar surface of epithelial cells. When viewed with light microscopy, these stages appear as dots. Meronts contain only four to eight merozoites. Some oocysts sporulate in situ and contain four sporozoites.

 

Figure 2.36: Life Cycle of Cryptosporidium

 

 Figure 2.37: Life Cycle of Cryptosporidium

Cryptosporidium is typically found in neonatal or young animals. Disease is not always present. Cryptosporidium, however, has been associated with clinical enteritis. In several hosts, including man and domestic animals, and with respiratory illness in man and domestic birds.

Diagnosis is facilitated by identifying oocysts inthe feces with phase-contrast microscopy and several staining procedures formerly used for acid-fast bacteria.

V. HAMMONDIA

Hammondia hammondi is a nonpathogenic of cats closely related to T. gondii. Its life cycle and structure are essentially the same as those of t.gondii with the following exceptions:

Differentiation of H. hammondi from T. gondii must be based on a life cycle study.

 

Figure 2.38: Life Cycle of Hammondia Hammondi
 

5.2.6 BESNOITIA

Coccidia of the genus Besnoitia have been found primarily in bovids in Africa, Asia, and southen Europe, equids in Africa and Mexico, reindeer and caribou in North America, rodents and opossums in the United States, and lizards and opossums in Central America. All these animals are infected with the cyst stage and therefore appear to be intermediate hosts. However, few life cycles are known. Cats have been definitive hosts for three species of Besnoitia. Cats shed unsporulated oocysts in the feces. Oocystssporulate, resembling those of Isospora. On ingestion of sporulated oocysts by a susceptible intermediate host, sporozoites excyst and multiply asexually into clusters of fusiform cells (tachyzoites) that initiate cyst development in connective tissue. These cysts are spherical, white, glistening, and thick walled. They contain many thousands of PAS-positive bradyzoites and grow to several millimeters in diameter. The wall is often 10 microns thick or thicker and may contain several host cell nuceli. Cysts develop in connective tissue throughout the body but especially in the skin, conjunctiva, mesentery, and scrotum. On ingestion of cysts by the definitive host, bradyzoites are released and initiate merogony and then gametogony and oocyst formation in the small intestine.

Acute lesions of besnoitiosis are associated with multiplication of tachyzoites in experimental infections and chronic lesions with the cyst stage in natural infections. Acute lesions are characterized by necrosi of infected tissue. Chronic lesions result from displacement of normal tissue by cysts and granulomatous inflammation associated with rupture of cysts. Most often there is no inflammatory reaction.

5.2.7 FRENKELIA

Coccidia of the genus Frenkelia have an obligatory two-host life cycle involving a rodent intermediate host(prey) and a raptorial bird definitive host (predator). Except for marked morphologic differences in the cyst stage, the life cycle is nearly identical to that of Sarcocystis spp.

Rodents are infected by ingestion of sporulated oocysts or sporocysts. Merogony occurs in the rodent liver and tissue cysts are found in the centrl nervous system. Mature tissue cysts can be macroscopic. They are multilobulated and surrounded by a thin wall, with many thousands of slender bradyzoites, which are infectious to the definitive host. After ingestion, bracyzoites enter the intestinal cells and form gametes, which develop into oocysts after fertilization. Oocysts sporulate in situ and are shed in the feces.

 

Figure 2.39 Life Cycle of Besnoitia

 

 Lesions are primarily associated with develipment of first generation meronts in the liver of rodents. Characteristic lesions include hepatic necrosis and perivascular cellular infiltration in numerous organs. Growth of tissue cysts in the central nervous system may result in pressure necrosis of surrounding neural tissue, with a resultant resorptive inflammatory response.

 

Figure 2.40: Life Cycle of Frenkelia

 

 

5.2.8. CARYOSPORA

Coccidia of the genus Caryospora are found primarily in birds and snakes. Members of the genus were once thought to infect a single host species. Recent studies show that species of Caryospora have two-host life cycles, in wich the hosts have a predator-prey relationship. There are owl-mouse and snake-mouse cycles. Unsporulated oocysts are shed in the feces of the predatory or definitive host (birds and reptiles). Sporulated oocysts contain a single sporocyst with eight sporotoites. Ingestion of sporulated oocysts by the definitive host results in merogony, gamogony, fertilization, and formation of oocysts in the intestinal epithelium. Ingestion of sporulated oocysts by the prey or intermediate host (rodents) results in extraintestinal merogony, gamogony, fertilization, sporulation, and formation of a caryocyst typically contining a single sporozoite in the tonge, dermis, and hypodermis. Ingestion of the prey whose tissues contain caryocysts results in merogony (two generations), gamogony, and oocyst formation in the intestine of the predator.

Little is know of the pathogenicity of Caryospora. Experimentally infected mice develop facial edema and some die. Clinical illness has not been reported for definitive hosts.

 

Figure 2.41: Life Cycle of Caryospora

 

5.3 MALARIAL AND MALARIAL-LIKE ORGANISMS

5.3.1 Terms used in Relation to Malaria:

Sporozoite

The infective stage passed in the saliva of the mosquito and formed inside an oocyst by the process of sporogony.

Schizont

The stage undergoing asexual division by multiple fission or segmentation. These may be found in the liver cells (preerythrocytic schizonts or in the erythrocytes (erythrocytic schizonts).

Merozoite

Is the product of division by schizogony.

Secondary exo-erythrocytic stage

This was the term used to denote schizonts developing in the liver as a result of invasion by merozoites from preerythrocytic schizont. It is now believed that reinfection of liver cells does not occur by pre-erythrocytc merozoites.

Trophozoite

Is the stage of the asexual form with an undivided nucleus, seen in the erythrocyte.

Microgametocyte

The male gametocyte which produces a number of microgametes.

Exflagellation

The process by which microgametes are formed frm a microgametocyte.

Macrogametocyte

The female gametocyte which produces a single macrogamete.

Zygote

The fertilized ovum.

Ookinete

The motile stage of the zygote preceding the oocyst stage.

Oocyst

The zygote after the formation of the cyst wall.

Sporogony

The sexual phase in the life cycle of certain protozoa. In Plasmodia this takes place in the mosquito vector.

Romanowsky stain

Mixtures of methylene blue, eosin and methylene azure. Giemsa, Leishman and Wrights are examples of Romanowsky stain.

Schuffner’s dots

Pinkish small and round stippling seen on P. vivax and P. ovale infected red cells, in Romanowsky stained films. They appear earlier and in greater numbers in P. ovale than in P. vivax.

Maurer’s dots

Coarse and irregular stippling seen on P. falciparum infected red cells in Romanowsky stained films.

Ziemann’s dots

Pinkish small dots sometimes seen in P. malariae infected red cells in Romanowsky stained films.

Incubation period

The interval between the entry of sporozoites and the first clinical manifestation.

Pre-patent period

The minimum time between the entry of sporozoites and the first appearance of parasites in red cells.

Latency

The duration between the primary attack of malaria and the relapse. There are no parasites in the circulation during this period.

Paroxyses

Bouts of fever due to the liberation of merozoites during the erythrocytic schizogony.

Recrudescence

Renewed manifestation of infection due to the survival of erythrocytic forms.

Relapse(Recurrence)

Renewed manifestation of infection due to the invasion of blood by merozoites from the late pre-erythrocytic stage (previously known as secondary exo-erythrocytic stage).

Re-infection

Renewed manifestation of infection not due to the original infection but resulting from subsequent fresh infection.

Malaria

A mosquito-borne disease of humans and other animals resulting from infection of the parenchynal cells of the liver and the red blood cells by apicomplexan parasites belonging to the genus Plasmodium.

5.3.2 PLASMODIUM

5.3.2.1 Classification

Figure 2.42: Malaria Parasite

 

5.3.2.2 Geographic distribution

5.3.2.3 Epidemiology

5.3.2.4 Life Cycle, Morphology and Terminology of the Different Stages

 

 

 

 

1. Segmenter; 2. Young trophozoite; 3. Older ring or trophozoite; 4. Erythrocytic Cycle; 5. Merozoite penetrates erythrocyte; 6. schizont; 7. Exoerythrocytic Cycle; 8. Trophozoite; 9. Renters reticulo-endothelial cell; 10. Merozoites released; 11. Segmenter; 12. Microgametocyte; 13. Sporozoite fr tissue (reticulo-endothelial cell); 14. Bite by Mosquito; 15. Macrogametocyte; 16. Schizogony (Asexual Cycle) In Vertebrate; 17. Sporogony (sexual cycle) In Mosquito; 18. Head of Mosquito; 19. Sporozoites enter salivary gland; 20. Oocyst ruptures, releasing sporozoites; 21. Sporulation of secondary masses to form sporozoites; 22. Repeated nuclear division in secondary masses; 23. Secondary masses formed in oocyst; 24. Growth and repeated nuclear division in oocyst; 25. Zygote passes between cells lining mosquito’s stomac to become an oocyst; 26. Zygote; 27. macrogamete; 28. Exflagellation; 29. fertilization; 30. microgamete.

 

5.3.2.5 Malaria: the disease

5.3.2.6 Pathology

Continuation of Figure 2.44

 5.3.2.7 Diagnosis

5.3.2.8 Treatment

5.3.3 HAEMOPROTEUS

Malaria-like parasites of pigeons, doves and quail. Several species have been described. Haemoproteus columbae is the most important

5.3.3.1 Classification

5.3.3.2 Geographic Distribution: Worldwide

 

Table 2.6: Differrential Diagnosis of Malaria Parasites

    

5.3.3.3 Epidemiology

5.3.3.4 Life cycle, Morphology and Terminology of the Different Stages

Figure 2.45: Life Cycle of Haemoproteus

  

5.3.4 LEUCOCYTOZOON

Leucocytozoon spp. are found in birds. Of over 70 named species, many are indistinguishable from one another; they are named because of being found in different host species. Their life histories are incompletely known. All species have insect vectors, such as midges and simuliid flies. Sporozoites in the salivary gland of the insect enter the circulation of the bird when the insect bites. First generation schizonts of most species then develop in hepatic parenchymal cells and when mature release thousands of tiny round merozoites that are thought to initiate a second generation in hepatic parenchymal and phagocytic cells throughout the body. Those in phagocytic cells usually become very large megaloschizonts. When mature, they release millions of tiny round merozoites that either initiate schizogony in hepatic parenchymal cells or enter circulating erythrocytes or leukocytes, where they develop into microgamonts or macrogametes. Those of some other species are thought to be round at one time and elongate at another. Sexual maturation, fertilzation, and sporogony take place in the insect after ingestion of infected blood.

For those species of Leucocytozoon that are pathogenic, the basic lesion is destruction of erythrocytes resulting in anemia. Inflammatory and necrotic foci may be found in the liver.

Diagnosis is primarily based on identification of gamonts or gametes in blood smears or of megalozchizonts in smears or sections of organs.

 

Figure 2.46: Life Cycle of Lekucocytozoon

 

5.3.5 BABESIA, THEILERIA, CYTAUXZOON  

5.3.5.1 BABESIA SPP.

Piriform, round or oval parasites of erythrocytes of mammals. Various species of ticks are the intermediate hosts. Babesia bigemina of cattle is the most important species. B. bigemina causes "Texas Cattle Fever", "red water fever" or hemoglobinuria.

5.3.5.1.1 Classification

  • 1. Phylum Apicomplexa
  • 2. Reproduction stages ("piroplasms") have apical complex
  • 3. Class Pirplasmea - all intraerythrocytic stages are pear-shaped organisms.

5.3.5.3.1.2 Geographic distribution: worldwide

  • 1. Babesia bigemina has been eradicated from the United States by rigorous tick control methods

5.3.5.1.3 Epidemiology

  • 1. Babesia bigemina is transmitted by ticks of the genus Boophilus.
  • 2. Boophilus annulatus - Texas cattle fever tick
    • a. Transmits babesiosis in the southern U.S.
  • 3. Transovarian transmission
    • a. Transmission of the organisms from adult female ticks to larvae, and nymphal ticks to through the ova

5.3.5.1.4 Life cycle, terminology and morphology of the different stages.

5.3.5.1.5 Pathology and Pathogenicity

  • 1. More severe in adult cattle than in calves
    • a. Rarely occurs in calves less than 1 year old.
    • b. Mortality is 50 to 90% if untreated
  • 2. Incubation period is 8 to 15 days
  • 3. Temperature rises to 106 to 108 F
  • 4. Malaise and anorexia
  • 5. Anemia
  • a. Severely anemic animals may die in 4 to 8 days
  • 6. Jaundice (Icterus)
  • 7. Hemoglobinuria

5.3.5.1.6 Immunity

  • 1. Sterile immunity
    • a. Complete immunity produces after survival of an initial infection.
  • 2. Premunition
    • a. Immunity that is dependent upon the continued presence of the parasite at low levels in the blood.

     

      Figure 2.47: Life Cycle of Babesia spp
 

G. Diagnosis

  • 1. Demonstration of piroplasms in erythrocytes in stained blood smears
  • 2. serology
    • a. CFA
    • b. IFAT
    • c. IHA
    • d. CF and IH are the more specific of the tests

H. Treatment

  • 1. Quinuronium sulfate (Acaprin, Ludobal)
  • 2. Diminazene (Berenil)

I. Control

  • 1. Regular dipping of cattle in an acaricide effectively eliminates the tick intermediate host.
  • 2. Artificial premunization of young animals with a mild strain of Babesia.

 

 

J. Other Species of Babesia are listed in Table 2.7

 

Host

Parasite

Distribution

Pathogenicity

Cattle

Babesia bovis

Europe, Russia,

Africa Pathogenic

 Horses

B. caballi

B. equi

Worldwide

Worldwide

Pathogenic

Pathogenic

Dog

B.canis*

B. qibsoni

Worldwide

Europe, Africa, Asia

Pathogenic

Pathogenic

Cat

B. felis

Africa, Asia, North America

Less patho-genic than B. canis

Man

B. diverqens

B. microti

U.S., Europe

Europe, U.S.

Pathogenic

Pathogenic

* May cause severe regenerative anemia. Clinical signs also include anorexia and fever.

 

5.3.5.2 THEILERIA

Small piriform parasites of red blood cells and lymphocytes of mammals. Theileria parva causes " East Coast Fever" , one of the most important diseases of cattle in eastern and central Africa.

5.3.5.1.1 Classification

  • 1. Phylum Apicomplexa
  • 2. All blood stages have apical complex
  • 3. Class Piroplasmea - pear- to rod-shaped (smaller than Babesia)

5.3.51.2 Geographic distribution: worldwide

5.3.5.1.3 Epidemiology

  • 1. Theileria spp. are transmitted by one,two or three host ticks.
  • 2. Theileria parva is transmitted primarily by the brown cattle tick Rhipicephalus appendiculatus
  • 3. Transstadial transmission
    • a. Stage-to-stage transmission, i.e. larval to nymph, nymph to adult.

5.3.5.1.4 . Life Cycle, Terminology and Morphology of the different stages.

See Figure 2.48.

 

5.3.5.2.5 Pathology and Pathogenicity

 

  • 1. Clinical syndrome associated with schizogony
  • 2. Incubation period 9-24 days
  • 3. Enlargement of lymph nodes near site of tick bite
  • 4. Fever (410 C)
  • 5. Anorexia
  • 6. Diarrhea
  • 7. Cough and mucous discharge from eyes and nostrils
  • 8. Leucopenia
  • 9. Anemia
    • a. Anemia is caused by red cell rupture and by immune-mediated events

5.3.5.2.6 Immunity

  • 1. Premunition
    • a. Immunity is based on parasite's continued presence.

     

Figure 2.48: Life cycle of Theileria parva

 

5.3.5.2.7 Diagnosis

  • 1. Samples of superficial lymph nodes from biopsy or necropsy -Giemsa stain
  • 2 Thin blood smear
  • 3. Serology
    • a. IFA
    • b. CF
    • c. HAX

H. Treatment

  • 1. Menoctone has been effective against parasites in tissue culture. Berenil is not effective against Theileria spp.

I. Control

  • 1. Control tick populations by frequent dipping, spraying, or dusting.

J. Other species of Theileria infect sheep, goats and wild ruminants: Some are patogenic; others are not.

 

5.3.5.3 CYTAUXZOON

Cytauzoonosis is a rapidly fatal disease of domestic cats caused by Cytauxzoon sp. The parasite is similar to Cytauxzoon in African ruminants. The intraerythrocytic forms are indistinguishable from Theileria spp.

 

5.3.5.3.1 Classification

  • 1. Phylum Apicomplexa
  • 2. Reproducing stages - ("piroplasms") have apical complex
  • 3. Class Piroplasmea - pear-shaped organisms

5.3.5.3.2 Geographic distribution

  • 1. Cytauzoon in cats has been reported from cats in Missouri, Arkansas, Texas, Louisiana, Florida and Georgia

5.3.5.3.3 Epidemiology

  • 1. The disease is usually found in feral or farm cats where ticks are numerous. Other Cytauxzoon-induced diseases are tick-borne.
  • 2. The disease has been reproduced experimentally by injection of blood, splenic, hepatic and pulmonary triturates, and lymph-node homogenates.

5.3.5.3.4 Life Cycle, Terminology and Morphology of the Different Stages

  • 1. The infected stage is thought to be inoculated when the tick feeds. Inital schizogony occurs in histiocytes in blood vessels. Later, intraerythrocytic forms indistinguishable from Theileria spp. are present. Are intraerythrocytic forms infective to the tick??

5.3.5.3.5 Pathology and Pathogenicity

  • 1. Presenting signs
    • a. Anorexia and depression
    • b. Gradual rise in temperature (as high as 40-410 C)
    • c. Anemia, icterus, dehydration just prior to death
  • 2. Postmortem findings
    • a. Dark, enlarged spleen
    • b. Enlarged, reddened lymph nodes. Some lymph nodes are petechiates
    • c. Lungs are diffusely reddened, consolidated and are petechiated
    • d. May or may not be petechial or ecchymotic hemorrhages on the epicardium. The pericardial sac may be filled with a gelatinous icteric fluid
  • 3. Histopathology
    • a. Vessels in spleen, lungs, liver, lymph nodes are filled with large basophilic histiocytes. The nucleus of these cells is usually displaced to one side and cytoplasm filled with fine or coarse appearing granules.

5.3.5.3.6 Diagnosis

  • 1. Samples of visceral organs obtained at biopsy or necropsy will contain characteristic histiocytes
  • 2. Thin blood smear - Giemsa stain

5.3.5.3.7 Treatment - none

5.3.5.3.8 Control

  • 1. Prevent cats from roaming tick-infested areas or remove ticks promptly after returning from such areas.