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(See genital system) "Discssion of other species which causes Nagan in Africa later."
larvae in equine (see intestine)
In horse, mule, donkey. Found in USA/1961 Miami Florida having been introduced from Cuba. Cases have been reported in GA, NV, MS, AK, TN, all in horses originating in Florida orPuerto Rico.
Morphology similar to B. bigemina signs are also similar but hemoglobinuria is rare - Incubation peiod 6-10 days. Symptoms variable from mild to sever.
In equine - Is more pathogenic than above. Four trophozoites are usually found in host cell and for this reason some writers have ued another generic name, Nutalli for this and other similar species. There may be as many as eight B. equi in a single host cell.
Pyriform - shaped trophozoites in red blood cells.--- about 2 microns, in pairs. B. equi --- classical shape is a maltese cross, i.e. 4 trophozoites.
Young horses are more resistant. USA outbreak in 1961. A tick, Dermacentro nitens, is the vector.
Great variations, Acute to chronic. Mild to fatal. Usually see fever, anemia and icters. Posterior paralysis with some cases. Recovered animals may become carriers. Older horses are more susceptible. Temperatures of 104 + 5 or more days leads to icterus.
Stained blood smear. Organisms are easiest to recover during the febrile stage. Geographic location, presence of ticks, clinical signs, etc. may lead to a presumptive diagnosis.
Acapren & Acriflavine. Phenamidino.
"Southern Cattle fever piroplasm" Host include, Ox, zebu, water buffalo, deer, - not found in North America (eradicated). In South and Central america, Europe, Middle East, North, Central and South Africa, Australia.
Trophozoites are piriform and occurs characteristically in pairs. Round forms are 2-3 microns in diameter and the elongate forms are 4-5 microns long.
Multiplication by binary fission in RBC or by schizogony, forming tetrads. Babesia is transmitted by ticks. The discovery of this fact - by Smith and Kilborne (1893) for B. bigomina of cattle was a milestone in the history of parasitology since it was the first proof that an Boophilus annulatus in US B. microplus in Australia, South and Central America etc and other species of ticks are involved in other parts of the world - Transmission takes place through the eggs in all species of ticks and stage to stage in Haemaphysals and Rhipicephalus.
Highly pathogenic in adult cattle but less so in calves. Incubation period 8-15 days or less. Signs include fever 106-108 F which persist for a week or more, dull, listless, failure to eat, stop ruminating and severe nemia - 75% of erythrocytes may be destroyed. Hemoglobinuria usually present. Animal become thin and emaciated Death may occur in 4-8 days/mortality 50-90% in untreated cases-calves less than 1 year are very seldom seriously affected - PM liver (yellowish brown color), Icterus and edenuatous tissues, watery thin blood - Urine in bladder usually red. Premunition follows recovery (may be sterile) No cross immunity between B. argentina.
Fever associated with hemoglobinuria, anemia and icterus is suggestive, but must be confirmed by finding organisms on staine blood smears.
Drugs which have been found to be effective are trypan blue (1-2% solution) 50-100 ml I.V. acriflavin (1% sol.), acaprin (.02 ml/kg of 5% (sol). See lecture notes-Dipoolu.
Tick control, and artifical premunition of Young animals with a mild strain before shipping endemic area.
Argentine cattle fever prioplasmosis similar to B. bovis and found in same countries as B. bigemina. Not in USA - considered to be more pathogenic than B. bigemina. Other species in ruminants are recorded.
Thielaeria parva and T. annulata in bovine the cause of "East coast fever" a highly fatal and one of the most important diseases of Africa (East coast). The form in the erythrocytes are predominantly rod shaped.
Multiplication forms occur in lymphocyteasand sometimes in endothelial cells and are common in lymphnodes and spleen known as Koch’s bodies. Transmission is by tickes (Rhipicaphalus).
Eperythrozoonosis organism- Rickettsia to 1.5 microns - on erythrocytes of cattle.
Anaplasmosis organism Rickettsia. In red blood cells of cattle and deer. To 0.8 microns.
Anaplasmosis organism. In red blood cells and plasma of sheep.
The disease is most troublesome in certain areas of the states (USA) where the natural blood sucking vectors such as ticks, flies and mosquitoes abound. Anaplasmosis has been experimentally transmitted from infected to susceptible bovine hosts by bites of many species of ticks, by horseflies and mosquitoes, (transmission is mechanical. Ticks ingest infected blood and transfer the infection to the susceptible host animal when feeding is resumed. Perhaps in certin areas more game animals, such as deer are carriers of anaplasmosis than is now realized and in such areas may be a major factor in perpetuating the disease. The interstate shipment of cattle has apparently facilitate spread of anaplasmosis within the U.S. in recent years.
It has been shown that certain ticks are capable of transovarian transmission of the infection through the ova to the succeeding larvae. It is evident that this occurs under natural conditions because the female tick after feeding, leaves the host and lays her eggs. Next generation of ticks may then transmit the infection to susceptible hosts, cattle and wild game such as deer. The transmission by biting files appears to be by a mechanical transfer of blood from infected to susceptible cattle. It hs been reported that it is necessary that horse flies and stable flies to feed on susceptible cattle within a period of a few minutes after having fed on infected cattle in order to transmit the diseas. Experimental transmission occurred only in the sucking mouth parts of the insect were wet with infective blood when feeding was begun on a suceptible animal.
Man has mechanically transmitted anaplasmosis by the use of contaminated needless or surgical instruments which were not cleaned and disinfected before repeating the procedures on susceptible animals. Transmissions of anaplasmosis have been reported following insanitary dehorning and also following the insanitary moval of horn tips (14 & 15). In addition to these modes of infection, transmission have been reported in the insanitary techniques of vaccination, bleeding for serological tests and castrating in herds where anaplasmosis carriers were present.
Following use of clean and disinfected dehorning instruments for each animal, spurting of blood should be stopped after each bovine is dehorned. If this is not done, it is obvious that a carrier of anaplasmosis cahn, when in close proximity to susceptible members of the herd, contaminate anaplasmosis in insanitary ear notching, and possible the use contaminated nose tongs.
The cause of anaplasmosis has generally been assumed to be Anaplasma marginale, a Rickettsia.
The most important symptom of anaplasmosis is an acute anemia. When jaundice is present it appears to be due to an obstruction of the normal flow of bile from the gall bladder in to the intestine and over production of bilirubin. The first three symptoms of anaplasmosis to appera are: abrupt decline in milk production in lactating cow, slight decrease in appetite and the intermittent inclination of the affected animal to recline and to stay apart from the herd. The temperature of the affected animal the first day these symptoms appear will be one to two degrees higher than the average temperature of other animals in the herd. This is especially so in the afternoon. At the time these symptoms appear the total red blood cell count will be approximately 4,000,000 per c.m.m. of blood. The average total red blood cell count of an adult bovine is 6,000,000. If the animal is affected with the acute form of this disease and not treated there will be a loss of approximately 1,000,000 red blood cells or more during each 24 hour period. If the bovine is affected with the peracute form of anaplasmosis it may die 24 to 36 hours after the first clinical symptoms appear. Very often animals with this form of the disease are found dead without being known to have been sick. As the anemia progresses in untreated cases the following symptoms apper: elevation of body temperature up to 1070 F accelerated pulse of 70 to 40 minutes, accelerated respiration of 60 to 80 a minute, followed by pale mucous membranes, complete or almost complete loss of appetite, atony of the rumen, constipation, jaundice (not seen the peracute form), dry muzzle, weakness, marked dehydration and muscular termors. Cattle unaccustomed to condinement and restraint and those of a nervous disposition are prone to fight. This is due to an anoxemia of the central nervous system.
During the recovery period from acute anaplasmois the following symptoms sometimes apear: dribbling of urine, drooling of saliva, excessive thirst and mucopurulent nasal discharge. The latter probably due to secondary invading bacteria. Abortions may or may not occur in advance pregnancies.
Anaplasmosis in certain stages, may be confused with acute leptospirosis, bacillary hemoglobinuria and Texas fever (piroplasmosis). However, these diseases are accompanied by coffee of blood colored urine which is not present in anaplasmosis cases. It also may be confused with anthrax; and with parasitism and poisonings of the gastronintestinal tract with sometimes causes anemia nad a jaundice.
Because erythrocytes with anaplasma bodies are rarely found in blood of cattle which have recovered from anaplasmosis such carrier animals cannot be detected by this means.
A complement fixation test for the detection of cattle affected with anaplasmosis has been developed.
It has been considered that the inoculation of anaplasmosis susceptible splenectomized calves with blood from cattle suspected to be carriers is positive means by which to prove the anaplasmosis status of the suspect. This is only true if the splenectomized calf develops anaplasmosis. In some instances the splenectomized calf develops anaplasmosis. In some instances the suspect, the calf of both animals will harbor a latent infection of eperythorzoonosis. The causative agent of eperythrozoonosis will often block out the causative agent of anaplasmosis indefinitely unless the calf is inoculated two or more times with blood from the suspect. In such instances the incubation period of anaplasmosis may vary from 50 to 100 or more days.
It cost stockman of the United States $3.4 billion in estimated production losses and $3.5 million in mortality losses annually. Mortality has been reported as high as 50 percent of the infected animals. Cattle which recover from anaplasmosis are immune to the disease but are permanent carriers. anaplasmosis has been referred to as gall sickness, bovine malaria and gallziekt. It was probably introduced into the United States by the Spaniards along with Texas fever. The disease is not transmissible to man but it has been reported that other ruminants, such as the deer, elk, antelope, buffalo, camel, black wildbeest, duiker, lesbok and goat are susceptible. It has been recently recognized in sheep in the United States.
Anaplasmosis was first observed in this country in 1893 during the investigational studies of Texas fever. However it was not recognized to be a separate disease entity at this time but the anaplasma bodies were described and were considered to be a stage in the life cycle of the causative agent to Texas fever. In 1910 an African investigator presented evidence that an unrecognized disease of cattle had been identified. It was observed that this malady was characterized by the presence of bodies on or near the margin of the red blood cells. these bodies have been considerded to be Rickettsiae and the cause of the disease . Because they were assumed to be the cause of the disease and due to their location and the fact that they werewithout cytoplasm they were disignated Anaplasma marginale and the disease anaplasmosis. A. marginale is the only species knownin U.S, while it has been found with A. central in Africa. The bodies vary in size from 0.2 to 0.9 microns (25,000 microns per inch).
Anaplasmosis was first recognized in the United States in 1913; however, the infection was proved to coexist with Texas fever.
It was first reported, uncomplicated with Texas fever, 1926 when it was observed in Southeastern Kansas. In 1928 it was reported in California and the investigator indicated that he had diagnosed anaplasmosis in California as early as 1925. In 1932 four forms of the disease--peracute, acute, subacute and chronic - were described. The chronic form appears as an aftermath of acute cases that are not treatedor treated late in the course of the disease. Young calves develop the mild form, however, if such animals are splenectomized and then administered infective blood the acute or peracute form develops.
Made on finding organisms on Giemsa - stained blood films of suspected host. Differentiation from other forms of anemia.
Tetracyline of oxytetracline given in not less than 3 mg/lb (6.6 mg/kg) of body weight is specific in single doses against E. suis. Chlortetracyline in drinking water at rate of 200 mg/gal m(50 mg /L) is effective in herd treatment.
In circulating leucocytes of canidae -world wide- appears as colonies of coccoid bodies (compact, grape like clusters) termed morulae, in mononuclear cells, most often monocytes. Transmission is by ticks (history of heavy tick Rhipicephalus sanguineus is an efficient vector stage-to - stage. symptoms for ehrlichosis include tropical canin panocytopenia", canine haemorrhagic fever" idiopathoc hemorrhagic syndrome and tracker dog disease.
Vary from mild, acute, febrile syndrome to severe chronic and often fatal disease. Thrombocytopenia, leucopenia, anemia and hemorrhage are associated with often fatal form. symptoms of fever, serous nasal and ocular discharge, anorexia, depression, loss of weight, increased erythrocyte sedimentation rate along with those listed above were observed 10-12 days following tick attachment (in experimental infections) in acute cases.
Difficult to diagnose clinically because signs vary from vey mild to severe, chronic and fatal - presence of organism in wBC (monocytes) confirms. The parasitic infection - symptoms may point toward possible infection - only 1% of the monocuclear cells may be infected in chronic cases - a specific indirect florescent test (IFT) for the detection of E. canis antibodies is available (effective 10-14 days after infection). Dogs which survive acute infection remain carriers (chronically infected with few clinical signs).
Control ticks - continuous daily oral administration of tetracycline hydrochlorida hydrochlorida at 6.6 mg/kg of body weight in endeic areas.
Dog, fox, cat, cyote, wolf - rarely reported from other hosts.
involve mosquitoes which ingest circulating microfilariae while feeding on infected host. Infective larvae are reached in about 2 weeks. (14-16 days) (8-10 days in tropics). Infection is by vector inoculation where the larvae develops for a time in the connective tissues etc. (2 mos.) They are present in the heart 2-4 months after infection, another 2-3 months required for maturation and microfilariae appear in about 6-8 months after infection.
History usually indicate gradual loss of weight, decreased exercise tolerance, cough aggravated by exercise, and in advance cases, dyspnea, increased temperature, abdominal fluid, and cynosis. In acute hepatic syndrome (postcaval) adult worms obstruct posterior vena cava causing sudden onset of critical signs, hemoglobinuria and death within 24-72 hours due to hepatic or renal fialire.
Identification of microfilariae in blood (knott’s test) Diffirentiate from Dipetalonema reconditum which complicate diagnosis do not exhibit microfilariae incirculation. Why?
Daily administration of diethylearbamazine orally begun prior to and continued for 2 months after the mosquito season - or year - round daily therapy in areas with cinuous mosquito breeding -what precautions are adhered to? Why? B. annual treatment for adults is an alternated method of prevention-others. Newest method include the use of Ivermectin once per month.
Arsenamide is the drug of choice - SGPT and BUN tests should be done for clinical case evaluation - see text. Dithiazanine iodide is given to remove microfilaiae - given 3-6 weeks following treatment, depending on clinical judgement. Levamisole has been given with some side (CNS) effects.
22. Dipetalonema reconditum - to 32 m.m. In dog - Subcutanerous tissues apparently cause non - pathological involvement, although fairly common, microfilariae confused with those of heart worm (see chart).
Considered to involve dog and cat flea
23. Spirocerca lupi - Esophageal worm - to 80 mm - In aorta wall of dog, fox, bobeat, wolf, (see esophagus).
24. Haemobartonella felis - "Feline infectious anemia organism" - Rickettsiae - In erythrocytes of cat - coccoid to rod forms measure from 0.8 microns to 1.5 microns respectively natural transmissions not exactly known but since it ma y be experimentlly transmitted by parenteral or oral transfer of infected blood, possible vectors are involved. A significant portion the cat population may carry the infection in a latent form which may be exacerbated in the presence of debilitaint diseases of stresses. Autoimmune anemia may be observed - any anemic cat may be suspected of having feline infectious anemia, fever (100-106 F)) Jaundice anorexia, depression, weakness and splemomegaly are common signs.
is confirmed by laboratory measures to identify parasites.
25. Aeulurostrongylus abstrusus: "Lung worm" - 20 9 mm - In pulmonary arteriolar wall (see respiratory system)
Parasites invaid blood cells and undergo development in endothelial cells producing cell alteration - cells become typically elongated or distroted. Severe anemia and hemorrhage are common symptoms. Black flies (simuliidae) transmits the parasites in most birds however biting midges (culicoides severe in this capacity for the species in chickens.
No satisfactory exist. However pyrimethamine in the dier or sulfadimethoxine of sulfaguinoxaline in dier or drinking water prevents infections with L. caellercyi.
