Parasites - Internal
Coccidiosis (Isospora and Sarcocystis species) is an enteric infection, traditionally associated with Isospora canis (dogs) and Isospora felis (cats) as potential pathogens. Other species of Isospora may be present. Strictly host specific, i.e., no cross-transmission.
Coccidia is one of the most commonly seen parasites in cats, and is most common in young kittens and more likely to be seen where conditions of poor sanitation, stress and crowding exist. Several references in veterinary literature suggest that almost every cat will become infected by coccidia at some point in their life. Cats acquire the parasite by ingesting any source that has been contaminated by infected cat feces or by ingestion of infected rodents or other meat sources. These organisms reproduce themselves inside the lining cells of the intestinal tract. As the new organisms emerge from these host cells, the intestinal cell is killed in the process. The life cycle of Coccidia takes only a few hours to a few days and new organisms are again passed in the feces. This cycle is the major cause of re-infection which may appear as a persistent infection.
Infected cats may exhibit weight loss, weakness, dehydration and diarrhea with possibly blood and/or mucus being present. Kittens, immunocompromised or otherwise weakened cats will have more severe symptoms. Older and otherwise healthy cats may exhibit no symptoms whatsoever.
Fecal examination for oocysts is required for definitive diagnosis. Albon is the most commonly used drug for treatment of Coccidia. In severe cases of diarrhea, fluid therapy may be necessary to correct dehydration and electrolyte balance.
Giardia (Giardiasis)Giardia are sometimes confused with worms because they invade the gastrointestinal tract and can cause diarrhea. They are not worms; instead, they are one-celled parasites classified as protozoa. Most cats that are infected with Giardia do not have diarrhea or any other clinical signs. When the eggs (cysts) are found in the stool of a cat without diarrhea, they are generally considered a transient, insignificant finding. However, in kittens and debilitated adult cats, they may cause severe, watery diarrhea that may be fatal.
A cat becomes infected with Giardia when it swallows the cyst stage of the parasite. Once inside the cat's intestine, the cyst goes through several stages of maturation and replication. Eventually, the cat is able to pass infective cysts in the stool. These cysts lie in the environment and can infect other cats. They may also be transmitted through drinking infected water.
Giardiasis is diagnosed by performing a microscopic examination of a stool sample. The cysts are quite small and usually require a special floatation medium for detection, so they are not normally found on routine fecal examinations. Occasionally, the parasites may be seen on a direct smear of the feces. A blood test is also available for detection of antigens (cell proteins) of Giardia in the blood. This test is probably more accurate than the stool exam, but it requires several days to get a result from the laboratory performing the test.The typical drug most commonly used to kill Giardia is metronidazole (Flagyl), an antibiotic-type drug. It is given for 5 - 7 days. Other drugs are also used if diarrhea and dehydration occur. If metronidazole is not effective, other drugs such as quinicrine, panacur, albendazole and furazolidone are all commonly used.
Giardia can also cause diarrhea in humans. Therefore, environmental disinfection is important. The use of chlorine bleach, one cup in a gallon (500 ml in 4 liters) of water, is effective if the surfaces and premises can be safely treated with it. Remember to use gloves for your protection and to thoroughly rinse the litter box before allowing the cat access so that it does injest any bleach or irritate its paws.
Cryptosporidium is still being assessed as an acute life-threatening coccidiosis (cryptosporidiosis) of neonatal kittens. Voluminous watery diarrhea is characteristic; autoinfection and continuing recycling within the lower intestinal tract results in a rapid loss of the mucosal lining. Cryptosporidia are the smallest of all coccidia-type parasites and attacks the intestines of cats and many other warm-blooded animals. Although many cats become infected, few show clinical signs other than severe diarrhea. Most cats with actual cryptosporidial illness will be FeLV positive or otherwise weakened. Usually, the primary symptom of infection is chronic, persistent and watery diarrhea, weight loss and a poor appetite.
Diagnosis is made by fecal analysis by sugar flotation (oocysts are acid- fast positive), fecal antigen detection tests, or fluorescent antibody tests.
Humans can become infected by cats and vice versa which is the most serious aspect of this type of infection. In cats, treatment with paromomycin has resulted in the resolution of signs and the cessation of oocyst shedding.
J. P. Dubey,M.V.Sc., Ph.D.
Coccidia are obligate intracellular parasites, normally found in the intestinal tract. Until recently, to veterinarians the term coccidia usually meant hosts-pecific parasites of the genera Isosporaand Eimeria. The Eimeria are normally found in herbivores and are considered spurious parasites of cats. Eimeria oocysts appear in feline feces as a result of either ingesting Eimeria-infected prey or coprophagy. Therefore, Eimeria are not considered further in this section.
Until 1970, little was known of the coccidia of cats. After the discovery of the coccidian phase of Toxoplasma gondii in the feces of cats, it was found not only that feline coccidia can infect many nonfeline hosts, but that some of them are zoonotic. Feline coccidia include the genera: Toxoplasma, Hammondia, Sarcocystis, Isospora(also called Cystoisospora), Besnoitia, and Cryptosporidium. They belong to the phylum Apicomplexa, class Sporozoasida, order Eucoccidiordia. Although there are numerous species of feline coccidia, to facilitate discussion they are arranged into four groups.
There is one recognized species in this genus,Toxoplasma gondii. It infects most species of warmblooded animals, including humans. Infection in cats is of particular interest because Felidae (domestic, and wild) are the only known definitive hosts for T. gondii and thus are the main reservoirs of infection. Toxoplasma gondii infections are common in most mammals worldwide.
'There are three infectious stages: (1) tachyzoites (rapidly multiplying forms also called trophozoites or endozoites); (2) bradyzoites (slowly multiplying forms, also called cystozoites) in tissue cysts; and (3) sporozoites in oocysts. Tachyzoites and bradyzoites occur in body tissues, whereas oocysts are excreted in feces.
Cats can acquire infection by three primary ways: carnivorism, ingestion of feces, and congenital infection. Of these three, carnivorism is the most efficient means of transmission of T. gondiiin the cat. Most cats become infected by eating infected tissues containing T. gondii tissue cysts.
After ingestion of tissue cysts by the cat, the cyst wall is dissolved by the digestive fluids in the stomach and small intestine. The released bradyzoitespenetrate the epithelial cells of the small intestine and initiate a series (types A to E) of genetically determined asexual generations followed by the sexual cycle. After the male gamete fertilizes the female gamete, a wall is formed around the fertilized female gamete to form an oocyst. Oocysts are unsporulated when passed in feces and are therefore uninfective. After exposure to air they sporulate and then contain two sporocysts, each with four sporozoites. Sporulation takes 1 day or more after excretion, depending on environmental conditions. The entire coccidian cycle of T. gondii can be completed within 3 days of ingestion of tissue cysts.
After the ingestion of tachyzoitesor oocysts, the formation of oocysts is delayed until 3 weeks after ingestion.' Details of the life cycles after ingestion of tachyzoites and oocysts are unknown, but presumably sporozoites and tachyzoites invade and multiply in intestinal and extraintestinal tissues and form bradyzoites in the tissues of cats. After cyst rupture, the bradyzoites return to the intestine and continue the cycle as if tissue cysts had been ingested.
The life cycle of T.gondii in extraintestinal tissues is the same for all hosts, including cats, mouse, and humans. After ingestion of infected tissues or oocysts, the bratlyzoites or sporozoites penetrate intestinal cells, multiply as tachyzoites, and spread to other organs. Tachyzoites multiply in almost any type of host cell until the cell is destroyed. The released tachyzoites repeat the cycle in new host cells and eventually encyst. Tissue cysts are formed in the brain, muscles, heart, and visceral organs and probably persist for the life of the host.'
Parasiternia during pregnancy can cause placentitis followed by spread of T. gondii to the fietus. Congenital infection can occur in cats as in other hosts. Congenital infection can be fatal in cats.
Pathogenesis of Disease
Toxoplasma gondiiusually parasitizes cats without producing clinical signs. Only rarely does it produce severe clinical manifestations. Most natural infections are probably acquired by ingestion of tissue cysts in infected meat. The bradyzoites from the tissue cysts penetrate' the intestinal epithelial cells and multiply in the lamina propria of intestine. Toxoplasma gondii may spread locally to mesenteric lymph nodes and to distant organs via lymph and blood.' Focal areas of necrosis may develop in many organs. The clinical picture is determined by the extent of injury to these organs, especially vital organs, such as the eye, brain, lung, liver, heart, and adrenals. Necrosis is caused by the intracellular growth of tachyzoites. Toxoplasma is not known to produce a toxin.
The host may die of acute toxoplasmosis but more often recovers with the acquisition of immunity coincident with the appearance of humoral antibodies. Inflammation usually follows the initial necrosis. By about the third week after infection, tachyzoites begin to disappear from visceral tissues and may localize as tissue cysts in neural and muscular tissues. Tachyzoites may persist longer in the spinal cord and brain than in visceral tissues because immunity is less effective in neural organs.
Why some cats become ill due to toxoplasmosis whereas others remain well is not fully understood. Age, sex, strain of T. gondii, and number of parasites may account for some of these differences. Toxoplasmosis is most severe during the neonatal period. Nothing is known of the sex and breed susceptibility of cats to clinical toxoplasmosis. Other unknown factors vaguely classified as stress may affect the results of T. gondii infection in a host. Concomitant infections, including feline leukemia virus and feline immunodeficiency virus (FIV), may make cats more susceptible to T. gondii infection. Serologic evidence indicates that concurrent FIV and T. gondii infections are prevalent in cats with uveitis. Reactivation of dormant T. gondii infection can occur in an immunosuppressed individual, for example, during antitumor chemotherapy. The mechanism of reactivation is not known because no drug is known to induce rupture of tissue cysts or growth of inhibited T. gondii.
Cats and Public Health
Not only the domestic cat, but other Felidae, such .as the mountain lion (Felis concolor), ocelot (F. pardalis), margay (F. weidii), jaguarundi (F. yagouaroundi), bobcat (Lynx rufus), Pallas cat (F. manul), and Asian leopard cat (F. bengalensis), can also shedT. gondii oocysts, and T. gondii antibodies have been reported in wild Felidae. Oocyst formation however, is greatest in the domestic cat (F. catus). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed and the number of oocysts may exceed 100,000 per gram of feces. Although cats of any age not previously exposed to T. gondii shed oocysts, oocyst formation is greatest in 6- to 14week-old kittens. Passively transferred antibodies from mother to kittens do not affect oocyst shedding and clinical signs of toxoplasmosis in cats. The oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying. However, oocysts are killed by heating to 70º C for 10 minutes. They can be transported by earthworms, cockroaches, and flies.
Cats are pivotal in the transmission of toxoplasmosis. Because of the danger of transplacental toxoplasmosis during pregnancy, a major public health concern is the risk of having cats in the household of a pregnant woman. To assess this risk, one needs to understand how cats become infected with T. gondii in nature. Epidemiologic data indicate that most cats become infected in nature soon after they are weaned, either by carnivorism or by sharing food brought by the mother cat. Therefore, T. gondii infection is higher in feral cats than in domestic cats. Under laboratory conditions, most previously uninfected cats shed oocysts after ingesting infected tissues, whereas less than half of those fed oocysts shed oocysts. Moreover, the number of oocysts shed after ingesting oocysts is far less than that after eating infected tissues. Once having excreted oocysts, cats usually do not shed oocysts again. Even when they do, the number of oocysts shed is negligible compared with that of a primary infection. Although cats immune to T. gondii have shed large numbers of T. gondii oocysts the second time after laboratory-induced superinfection with Isospora felis, this phenomenon is probably not important epidemiologically because most cats become infected with I. felis early in life and maintain immunity to I. felis by constant low-level reinfections.
Cats prefer to defecate in soft ground and like to hide their feces. Unless cats are sick, little or no feces stick to their anal area. Because of their licking (grooming), fecal matter is rarely found on cat fur. Moreover, cats are usually not diarrheic during the period in which they are shedding' oocysts. Therefore, the possibility of oocysts sticking to cat fur is minimal, as is the possibility of transmission to humans via touching or caring for a cat. The chance of becoming infected via soil contaminated by a feral cat is greater than that from an indoor cat because feral cats usually hunt.
Because cats may not develop antibodies during the oocyst-shedding period, a serologic examination of the cat does not provide any useful information regarding the transmissibility of toxoplasmosis via a particular cat. However, if a cat is serologically positive, it probably has shed oocysts. Thus, a serologically positive (immune) cat may be less of a danger than a serologically negative (nonimmune) cat. However, both immune and nonimmune cats can shed T. gondii oocysts; appropriate precautions should therefore be taken to avoid contact with feline feces. For additional information regarding prevention of human infection, see the section, Prevention and Control.
The prevalence of T. gondii oocysts in feline feces is low.' Therefore, chances of detection of T. gondii during a routine fecal examination are slim. Except in a few instances, less than 1 percent of cats have been found shedding oocysts; this is especially true in the United States.
Subclinical and Clinical Infections
Serologic surveys indicate that T. gondii infections are common worldwide. Approximately 30 percent of cats in the United States have T. gondii antibodies. The prevalence increases with age of the cat because of chance of exposure rather than age susceptibility. Prevalence of T. gondii infection also varies with the lifestyle of cats surveyed. It is higher in free-roaming cats that hunt for their food than in domestic cats.
Clinical toxoplasmosis in cats was first reported from a cat in New York in 1942. Since then fatal feline toxoplasmosis has been reported from many countries. However, most cases were reported from the United States (e.g., the Angell Memorial Animal Hospital, Boston), probably because of awareness of the disease and diagnostic facilities.As most reported cases in cats have been diagnosed after their death, little is known concerning clinical signs. Anorexia, lethargy and dyspnea caused by pneumonia are the most common signs. Uveitis is also considered a common clinical manifestation, which is supported by a seroprevalence of T. gondii in cats with uveitis ranging from 74 to 80 percent. Other clinical signs are icterus, vomiting, fever, diarrhea, disorders of the central nervous system, and enlarged abdomen. These signs may persist for a few days or several months, although some cats may die suddenly without prior clinical signs. Virtually any cell or organ may be affected by T. gondii, ranging from the skin to nictitating membrane. Therefore, clinical signs are varied, depending on the organ affected. Of 100 cats with histologically diagnosed toxoplasmosis, were considered to have generalized toxoplasmosis, mainly pulmonary, 16 abdominal, 2 hepatic, I pancreatic, 1 cardiac, 2 cutaneous, and 7 neurologic, and 9 had neonatal toxoplasmosis. An encephalitic cat may be totally depressed or manifest hysteria. Pneumonia, usually presenting for dyspnea, is the most consistent finding and can be rapidly fatal within 1 to 2 days. Clinical toxoplasmosis has been reported concurrently with hemobartonellosis, feline leukemia virus, feline infectious peritonitis virus, FIV, bacterial infections, and noninfectious conditions.
Clinical toxoplasmosis is most severe in transplacentally infected kittens. Affected kittens may be born dead or may die before weaning. They may continue to suckle until death. Hepatitis is the most consistent finding; as much as 75 percent of liver may be destroyed due to T. gondii. Encephalitic kittens may sleep most of the time or keep crying and may be unable to suckle.
Ocular manifestation result from uveitis involving both anterior and posterior chambers and include iritis, iridocyclitis, keratic precipitates, retinochoroiditis, detachment of the retina, and occasionally conjunctivitis and infection of the nictitating membrane. Uveitis of the anterior segment is the most common lesion of toxoplasmosis in cats with oplithalmitis. Retinitis may be present both in tapetal and nontapetal areas and involve one or both eyes. Lesions may be large enough to be grossly visible. Hemorrhage and opacities of the vitreous may be seen, depending on the stage of the disease. Secondary glaucoma may also occur.
The predominant lesion in toxoplasmosis is necrosis, particularly in the lungs; it may be grossly visible in the lungs, liver, spleen, mesenteric lymph nodes, or pancreas. Granulomatous enlargement of the mesenteric lymph nodes and small intestines, cholangioliepatitis with hyperplastic bile ducts, and peritonitis have been observed. Neural lesions are usually small and are characterized by vasculitis, gliosis, and necrosis. Very rarely the lesion is macroscopic. Inflammatory lesions usually consist of infiltrations by macrophages and lymphocytes.
Radiographs can aid in the diagnosis because the lungs are usually involved in cats sick with toxoplasmosis. Radiographic changes include diffuse symmetric or patchy opacities in the lungs, usually bilateral.
Other laboratory aids include determinations of serum ALT (SGPT), creatine phosphokinase, bilirubin, lactate dehydrogenase and lipase, and white blood cell counts Serum enzymes indicative of tissue damage may be elevated, depending on the location (liver, pancreas, skeletal muscle) and extent of tissue necrosis. There may be leukopenia or leukocytosis. Fecal examination for the detection of T. gondii oocysts is not likely to be rewarding because oocysts are generally excreted for a few days before the cat becomes sick. Occasionally, oocysts may be found in feces of congenitally infected kittens and in adult cats.
Serologic tests for T. gondii-specific antibodies, especially immunoglobulin M (IgM) antibodies, are diagnostically useful; however, antibody titers alone do not provide a definitive clinical diagnosis because they do not differentiate previous infection from active infection, and they do not correlate with severity of disease. Available serologic tests include direct hemagglutination (HA), indirect hemagglutination (IHA), latex agglutination (LA), modified agglutination (MA), enzyme-linked immunosorbent assay (ELISA), and indirect fluorescent antibody (IFA) tests. During T. gondii infection, IgM antibodies appear early and generally do not persist past 3 months after infection; thus, IgM titers (of greater than or equal to 1: 256) correlate with recent or active infection. By contrast, IgG antibodies appear by the fourth week postinfection and persist for months to years, sometimes at very high titers (greater than 1: 65,000) in subclinical infections. Thus, an elevated IgG titer merely indicates previous infection in most cases. A fourfold rise in the IgG titer in paired serum samples taken 2 to 4 weeks apart suggests acute infection, but not necessarily clinical disease. To evaluate titer rise, both samples must be assayed together in the same test run because titers may vary two- to fourfold from day-to-day analytical variation. Agglutination tests JHA, LA) are easy to perform and readily available cornmercially; however, these are of limited value because they primarily detect the late-appearing, long-duration IgG antibodies, and they often fail to identify those cats with only IgM antibodies. Coinfection with FIV is common in cats infected with T. gondii, and up to one-half of these cats have only an IgM antibody response. This is because FIV coinfection affects T. gondii-specific humoral responses causing a delayed shift from IgM to IgG for as long as 9 months. The development of ELISA tests for detection of T. gondii-specific antigen and IgM antibodies by Lappin and associates has made the diagnosis of recent and clinically active infection more accurate. The T. gondii antigen and IgM ELISA tests are available on a mail-in basis from the Toxoplasmosis Serology Laboratory of the College of Veterinary Medicine at Colorado State University, and from the Infectious Disease Laboratory of the College of Veterinary Medicine at University of Georgia. In summary, diagnosis of clinical toxoplasmosis should be based on serologic evidence (e.g., ELISA for T. gondii-specific IgM and antigen, rising IgG titer) combined with clinical signs and possibly response to an anti-Toxoplasma drug such as clindamycin. In cats with uveitis, simultaneous evaluation of serum and aqueous humor for T. gondii-specific antibodies and antigens may aid the diagnosis of ocular toxoplasmosis.
Toxoplasma may be found in impression smears or in tissue sections. Any blood stain can be used to stain T. gondii in smears. Impression smears of lung or liver needle biopsy material or ascites may be useful in antemortem diagnosis. Cerebrospinal fluid may contain T. gondii in neurologic cases.
Toxoplasma gondii can be found in histologic sections.. The mere presence of T. gondii tissue cysts without lesions does not indicate illness due to toxoplasmosis. Demonstration of tachyzoites, on the other hand, does suggest clinical toxoplasmosis. Immunohistochernical staining can facilitate recognition of T. gondii in tissues. Other Toxoplasma-like parasites that can cause clinical disease in cats should be distinguished from T. gondii in sections.
Little is known of the efficacy of various drugs in treating naturally occurring toxoplasmosis in cats because antemortem diagnosis has been made in so few cases. Clindamycin HCI (Antirobe; Upjohn) appears to be an effective and well-tolerated antitoxoplasmic drug for cats, given orally at a dosage of 25 mg/kg q12h for 14 to 21 days.
Sulfadiazine and pyrimethamine (Daraprim) are two drugs widely used in the treatment of toxoplasmosis in humans. They act synergistically on multiplying T. gondii by blocking the metabolic pathway involving the p-aminobenzoic acid and folicfolinic acid cycles, respectively. The commonly used sulfonamides-sulfadiazine, sulfamethazine, and sulfamerazine-are all effective against toxoplasmosis. Whereas these drugs have beneficial action when given in the acute stage of the disease process (when there is active multiplication of the parasite), they generally will not eradicate T. gondii. Sulfonamides are excreted within a few hours of administration; therefore, they have to be administered daily in divided doses (e.g., four doses, 60 to 120 mg/kg body weight of sulfadiazine). However, pyrimethamine (1 mg/kg body weight daily) can be given daily or every other day. Pyrimethamine is bitter and can produce frothing when administered orally to cats. For parenteral administration, pyrimethamine can be dissolved in 85 percent lactic acid or 5 percent acetic acid, refrigerated, and diluted with saline solution as needed. Treatment should be started as soon as the probable diagnosis is established because the disease could be fatal within a few days.
Trimethoprim (Tribrissen), another antitoxoplasmic drug, is available in combination with sulfadiazine as an oral suspension. However, its efficacy against toxoplasmosis in cats is unproven.
Good personal hygiene should be-practiced when treating the ill cat. Tachyzoites may be excreted in vomitus, feces, urine, skin exudates from ulcers, and possibly from oral secretions or exudates.
Prevention and Control
Toxoplasmosis is an important zoonotic disease (see the section, Cats and Public Health). To prevent human infection, the hands should be washed thoroughly with soap and water after handling meat. All cutting boards, sink tops, knives, and other materials that come in contact with uncooked meat should be washed with soap and water because the stages of T. gondii in meat are killed by water. The meat of any animal should be cooked to 70ºC before human or animal consumption, and tasting meat while cooking it or while seasoning homemade sausages should be avoided. Pregnant women, especially, should avoid contact with cat feces, soil, and raw meat. Pet cats should be fed only dry, canned, or cooked food. Cat litter should be emptied every day, preferably not by a pregnant woman. Gloves should be worn while gardening. Vegetables should be washed thoroughly before eating because they may have been contaminated with cat feces. Expectant mothers should be aware of the dangers of toxoplasmosis.
Although certain drugs can prevent or minimize oocyst shedding in cats, chernoprophylaxis has not proved practical. Because most cats become infected by eating infected tissues, cats should never be fed uncooked meat, viscera, or bones, and efforts should be made to keep cats indoors to prevent hunting. Trash cans should be covered to prevent scavenging. Freezing is an effective way to kill tissue cysts in meat. Cats should be spayed to control the feline population on farms so as to reduce entry of T. gondii into the food chain. Dead animals should be removed promptly to prevent scavenging by cats and other animals. A vaccine to prevent toxoplasmosis in humans or animals is not yet available.
RoundwormsAs their name implies, these are worms which have round bodies. On average, they are about 3 - 5 inches (7 -12 cm) long. They live in the cat's intestines and consume partially digested food. Unlike hookworms, they do not attach to the intestinal wall; rather, they literally swim in their food. Roundworms, sometimes called ascarids, pass moderate numbers of microscopic eggs which are found in the cat's stool. Like hookworm eggs, they must be found with a microscope.
The major source of roundworm infection for kittens is the mother's milk. Roundworm larvae (immature worms) may be present in the queen's mammary glands and milk throughout the period of nursing the kittens.
Both kittens and adult cats may become infected by swallowing roundworm eggs which contain infective larvae. The larvae hatch out in the cat's stomach and small intestine and migrate through the muscle, liver, and lungs. After several weeks, the larvae make their way back to the intestine to mature. When these worms begin to reproduce, new eggs will pass in the cat's stool, and the life cycle of the parasite is completed. Obviously, roundworm eggs passed in one cat's stool may be infectious to other cats. Interestingly, a large number of other animal species have been found to harbor roundworms and represent potential sources of infection for cats. These include cockroaches, earthworms, chickens, and rodents.Roundworms are not highly pathogenic (harmful) to adult cats, but large numbers can cause weight loss and a pot-bellied appearance to kittens and weak adults. Decreased appetite, vomiting or diarrhea will be observed on occasion. Kittens will sometimes die with serious roundworm infections. Roundworms are diagnosed by a microscopic examination of the cat's stool. They pass a moderate number of eggs, so examination of more than one stool sample may be necessary to find them. Occasionally, the mature worms can be found in the cat's stool or vomit. Treatment is quite simple. Several very safe and effective drugs are available to kill roundworms in the intestine. Some of these drugs temporarily anesthetize the worms so that they pass out of the cat with a normal bowel movement. The live or dead worms are found in the stool. Because of their large size, they are easily seen. At least two or three treatments are needed; they are typically performed at 2 - 4 week intervals. None of these treatments will kill the immature forms of the worm or the migrating larvae. Do not use "dewormers" commonly sold over the counter, often these chemicals will make the cat ill and fail to resolve the problem. Over-the counter-wormers can be very toxic and irritating to your cat and should be avoided. These medications are often very specific so a "one size fits all" approach is no longer acceptable and may actually be dangerous. Also, if other problems secondary to a parasitism have occurred, such as dehydration, worming alone will not cure your cat.. The safest and most effective drugs can be prescribed only by your veterinarian.
The eggs are highly resistant to most commonly used disinfectants and to even harsh environmental conditions. Therefore, removal of the cat's stool is the most effective means of preventing reinfection. A 1% solution of household bleach can be used to remove the sticky outer coating of the eggs, making it easier to rinse them away. This does not, however, kill the eggs. Remember the obvious limitations about where bleach may be safely applied. If bleach is used in the cat's litterbox, be sure to rinse it completely since bleach is toxic to cats.The roundworms of both cats and dogs pose a health risk for humans. As many as 10,000 cases of roundworm infection in humans have been reported in one year. Children, in particular, are at risk for health problems should they become infected. A variety of organs may be affected as the larvae migrate through the body. In suitable environments, the eggs may remain infective to humans (and to cats) for years. Prevention and Control
Adult hookworms pass hundreds of microscopic eggs in the cat's stool. The eggs are invisible to the naked eye. Larvae (immature worms) will hatch from the eggs and remain in the soil for weeks or months. If the cat swallows any of these larvae, hookworm infection will be established. The larvae may also burrow through the cat's skin and migrate to the intestine, where they will mature and complete their life cycle.
In dogs, prenatal infection (infection prior to birth) may be a significant problem. Puppies may become infected by the placental blood flow and then later through the mother's milk. Prenatal infection has not been demonstrated to occur in kittens.For cats, the most significant problems appear related to intestinal distress and anemia. Blood loss results from the parasite sucking blood from intestinal capillaries. A blood transfusion may be needed in some cats because of the rather severe anemia which can be produced by hookworms. The presence of pale gums, diarrhea, or weakness might suggest the need to specifically determine the cat's red blood cell count. Some cats experience significant weight loss with hookworm infection.
In dogs, skin irritation and itching can be one of the common signs of a heavily infested environment. The larvae burrow into the skin and cause the dog a great deal of discomfort. The most common hookworm of cats does not appear to have this type of burrowing behavior.Hookworms are diagnosed with a microscopic examination of a small stool sample. Since the eggs are produced on a daily basis, hookworm infection is usually fairly easy to diagnose. There are several very effective drugs that will kill hookworms. These are given by injection or orally and have few, if any, side-effects. However, these drugs only kill the adult hookworms. Therefore, it is necessary to treat again in about 2 - 4 weeks to kill any newly formed adult worms that were larvae at the time of the first treatment. Do not use "dewormers" commonly sold over the counter, often these chemicals will make the cat ill and fail to resolve the problem. Over-the counter-wormers can be very toxic and irritating to your cat and should be avoided. The safest and most effective drugs can only be prescribed by your veterinarian. Since the cat's environment can be laden with hookworm eggs and larvae, it may be necessary to treat it with a chemical to kill them. There are several available that are safe to use on grass. The type of hookworms which infect cats do not infect humans; however, the larvae can burrow into human skin. This causes itching, commonly called ground itch, but the worms do not mature into adults. Direct contact of human skin to moist, infected soil is required. Fortunately, this occurs rarely if normal hygiene practices are observed. Prevention and Control
How cats get tapeworms First, tapeworm eggs must be swallowed by flea larvae (an immature stage of the flea). Contact between flea larvae and tapeworm eggs is thought to occur most frequently in contaminated bedding or carpet. The life cycle of the tapeworm cannot be completed unless the flea swallows tapeworm larvae. Next, the cat chews or licks its skin as a flea bites; the flea is then swallowed. As the flea is digested within the cat's intestine, the tapeworm hatches and anchors itself to the intestinal lining.
Tapeworms are not highly pathogenic (harmful) to your cat. They may cause debilitation and weight loss when they occur in large numbers. Sometimes, the cat will scoot or drag its anus across the ground or carpet because the segments are irritating to the skin in this area. This behavior is much more common in dogs than cats. The adult worm is generally not seen, but the white segments which break away from the tapeworm and pass outside the body rarely fail to get an owner's attention! Occasionally, a tapeworm will release its attachment in the intestines and move into the stomach. This irritates the stomach, causing the cat to vomit the worm. When this happens, a worm several inches in length will be seen.
Tapeworm infection is usually diagnosed when the white, mobile segments are seen crawling on your cat or in the stool. Tapeworms are not usually detected by the routine fecal examination performed by the veterinarian. Because of this, veterinarians depend on the owner to notify them of possible tapeworm infection in the cat.Treatment is simple and, fortunately, very effective. A drug which kills tapeworms is given, either orally or by injection. It causes the tapeworm to dissolve within the intestines. Since the worm is usually digested before it passes, it is not visible in your cat's stool. These drugs should not cause vomiting, diarrhea, or any other adverse side-effects. Do not use "dewormers" commonly sold over the counter. Over-the counter-wormers can be very toxic and irritating to your cat and should be avoided. The safest and most effective drugs can be prescribed only by your veterinarian. Control of fleas is very important in the management and prevention of tapeworm infection. Flea control involves treatment of your cat, the indoor environment and the outdoor environment where the cat resides. If the cat lives in a flea-infested environment, reinfection with tapeworms may occur in as little as two weeks. Because the medication which treats tapeworm infection is so effective, return of the tapeworms is almost always due to reinfection from the environment. Pinworms Tapeworms and pinworms look very similar. However, contrary to popular belief, pinworms do not infect cats or dogs. Any worm segments seen associated with cats are due to tapeworms. Children who get pinworms do not get them from cats or dogs.
Feline tapeworms infections are not common or likely in people. A flea must be ingested for humans to become infected with the most common tapeworm of cats. Most reported cases have involved children. The most effective way to prevent human infection is through aggressive, thorough flea control. The risk for infection with this tapeworm in humans is quite small but does exist One less common group of tapeworms, called Echinococcus, is of particular concern as a threat to human health. These tapeworms cause very serious disease when humans become infected. This parasite is harder to diagnose than the tapeworm caused by fleas because the segments are small and not readily seen. Hunters and trappers in the north central United States and south central Canada may be at risk for infection by this worm if strict hygiene is not observed. Foxes and coyotes (and the wild rodents upon which they prey) are important in the life cycle of this parasite. Dogs and cats may also become infected if they eat rodents carrying the parasite. Another good reason to keep your cat indoors and supervised while outdoors.
Whipworms are a very long, slender worm that can reach 4 inches in length. Inlike tapeworms, hookworms, and roundworms which inhabit the small intestine, whipworms colonize the large intestine, particulary the cecum and colon of the cat. Adult worms pass a football-shaped egg which, when ingested orally, hatches into a larvae, develops into an adult worm and attaches to the colonic wall of the animal. Signs of illness will often be minimal in light infestations, but if enough worms are present, diarrhea, often with blood and mucus and a loss of weight may occur. Your veterinarian may diagnose this as a Whipworm Colitis. Infection by whipworms in cats, however, is quite rare.