4/6/2017
Cairo University Faculty of Veterinary Medicine Department of Medicine and Infectious Diseases
INFECTIOUS DISEASES OF DOGS AND CATS
Course 453
2017
PARASITIC DISEASES OF DOGS & CATS Dr. Soliman Mohammed Soliman Hasan Lecturer of Infectious Diseases Dept. of Medicine and Infectious Diseases Faculty of Veterinary Medicine Cairo University
1 4/6/2017
Infectious Diseases of Dogs and Cats
PARASITIC BACTERIAL VIRAL 1-Toxocariasis. 1- Canine brucellosis. 1- Rabies. 2- Dipylidiasis. 2- Kennel cough. 2- Canine Distemper. 3- Canine Babesiosis. 3- Leptosirosis. 3- Canine Parvovirus. 4- Canine Ehrilichiosis. 4- Feline leprosy. 4- Infectious canine hepatitis. 5- Ear mange. 5- Salmonellosis. 5- Cat Flu. 6- Red Mange. 6-Botulism. 6- Feline Infectious Peritonitis. 7- Sarcoptic Mange. 7-Feline Infectious anemia. 7- Feline Panleukopenia. 8- Isosporosis. 8- Feline Leukemia Virus. 9- Neosporosis. FUNGAL 10- Toxoplasmosis. 1-Ringworm. SYNDROME 11- Ticks. 2-Nasal Aspergillosis. 1- Fading Puppy syndrome. 12- Flea. 2- Fading Kitten Syndrome.
2 4/6/2017
CLASSIFICATION OF IMPORTANT PARASITIC DISEASES OF DOG AND CAT
External Internal Blood
Nematodes: Micro: Inside RBCs: Ascairs (Toxocara) Mite infestation. Babesia. Demodex, Sarcoptes and Cestodes: Psorptes. Dipylidium caninum Inside WBCs: Erlichia. Macro: Protozoa: 1- Tick infestation. 1- Toxoplasma. 2- Fleas. 2- Isospora (coccidia). 3- Lice infestation. 3- Neospora.
ASCARIASIS (TOXOCARIASIS)
3 4/6/2017
Ascaris is a nematodal worm of small intestine affecting dog, cat (of zoonotic importance, visceral larval migrans) commonly occurs in puppies and kittens characterized by enlargement of abdomen with presence of adult worms in vomitus or faeces.
Etiology
• Toxocara canis infect dog and fox. • Toxocara cati infect cat and wild felidae. • Toxocara leonina infect dog, cat, fox, wild felidae and canidae.
Mode of infection and Transmission 1. Ingestion of contaminated food or water with egg containing L2 2. In bitch: may reach fetus transplacental 3. Through milk (colostrum) Infective Stage
.Egg containing embryo (L2)
4 4/6/2017
Life cycle (21-28 days)
Adult worm in small intestine (puppies and adults)
Eggs pass in feces
Embryonated eggs (egg containing 2nd larval stage) in the environment
Ingestion of contaminated food and water
2nd larval stage penetrate duodenal wall as 3rd stage
Hepato-pulmonary migration (blood → liver → heart → lung)
3rd larval stage expelled with sputum and re-swallowed to reach small intestine and become mature which secrete eggs with faeces
OR 2nd larval stage may migrate via placenta (transplacental infection) to infect fetuses or may pass to milk or colostrum to infect newly born pups
5 4/6/2017
Clinical signs
1. Progressive emaciation (with normal appetite) 2. Enlargement of abdomen "Pot belly" (worms that causes hypoproteinaemia and ascites) 3. Fever (due to pneumonia as secondary infection 39.5 – 40 °C) 4. Infected animals have alternating periods of diarrhea and constipation 5. Vomiting and Diarrhea (may contain snake like worms) 6. Icterus (obstructive jaundice if the adult obstructs the bile duce/ rarely hepatic jaundice if there is damage to liver tissue) => not a very common sign
Clinical signs
7. Nervous signs (due to false migration of larva from heart to brain or accompanied the dead worms byproducts) 8. Rough coat (loose and dull) 9. A characteristic breath odor of acetone. 10.Coughing and nasal discharge 11.Fading puppy/ kitten syndrome (intestinal obstruction and pneumonia due to invading larvae that causes death during first few days of life) 12.Transplacental infection results in stillbirth due hepato- pulmonary and placental damage.
6 4/6/2017
Pot-belly (Ascaris Infested Puppy)
Adult Worms Of Toxocara In Dog Stool
7 4/6/2017
PM Enteritis Snake like worm in small intestine Pneumonia
Diagnosis
• A history of weight loss, pot belly and presence of snake like worms in faeces or vomitus. • demonstration of characteristic ascaris egg in faeces by direct smear or concentration Floatation Technique as a circular, thick wall egg with single, large, opaque embryo
8 4/6/2017
Treatment
Specific treatment: 1. Piprazine salts (drug of choice) orally. 2. Albendazole 3. Dorontal plus (contains Praziquantel active against cestodes as Dipylidium/ Pyrantel pamoate active against hookworms and ascaris and acts on the cholinergic receptors of the nematode resulting in spastic paralysis/ Febantel active against nematodes and blocks the parasite's energy metabolism, leading to energy exchange breakdown and inhibited glucose uptake) 1 tab/ 10 kg and repeated after 2 weeks 4. Revolution® pour on which is used on skin and effective against external parasites and round worms of dog and cat. 5. Bitches should be treated by daily dose of Fenbendazole as 25 mg/Kg for about 3 weeks before and 2 days after parturition. Also treatment of lactating bitch is recommended if puppies are infected. 6. Fluvermal syrup which interferes with the cellular tubulin formation in the worms leading to disturbance in the glucose uptake (dose of 3 days then repeated after 2 weeks).
Symptomatic treatment: 1. Antibiotic (pneumonia) 2. Antipyretic (fever) 3. Laxative (after anthelmintic) 4. Vitamins and minerals 5. Tranquilizers in case of nervous manifestation.
Control
• Treat all puppies in range and the dam • Give prophylactic dose (periodical deworming) every 3 – 6 months and before pregnancy, parturition and weaning
Public Health Importance
. Visceral larval migrans: (Toxocara canis) . Human accidentally ingests the infective stage while playing with puppies and the signs differ according to the organ to which it migrates
9 4/6/2017
TAPEWORM INFECTIONS “DIPYLIDIASIS”
It is a parasitic disease of dog, cat and man caused by cestode (tapeworm) called Dipylidium caninum, is transmitted by flea characterized clinically by diarrhea, emaciation, coilc, mild hyperesthesia with muscle twitching, convulsions and epileptiform fits occuring in heavy infestation.
10 4/6/2017
• Etiology: Dipylidium caninum • Final host: Dog and Cat • Intermediate host: Flea • Infective stage: Cysticercoid • Mode of infection: Ingestion of adult flea containing cysticercoid
Life Cycle
Adult worm in small intestine of final host ↓ Eggs pass out in feces (in gravid proglottids in egg capsule) ↓ Rupture of capsule and ingestion of egg by flea ↓ Eggs ingested by the flea, onchosphere is liberated after the ingestion of the eggs by intermediate host (Flea larva) so, Cysticercoid in the adult flea ↓ Ingestion of flea containing cysticercoids which mature to adult worm in small intestine 2-3 weeks post-infection
11 4/6/2017
Clinical signs
1. Infected dog become greedy in food 2. The coat become rough and the emaciation is present. 3. Diarrhea has been noted but subsides in a few days 4. Irritation in anal region due to passage of gravid proglottides lead to animal assumes the sitting position and draws its anus over the ground. 5. Fresh dried segments are frequently noted in stool or attached to the perianal region of infected dogs. 6. Irritation of the abdomen is sometimes apparent, is manifested in rolling or dragging over the ground, bite at the abdomen in an attempt to reduce the itching 7. Mild hyperesthesia with local muscles twitching and frequently paroxysms 8. Convulsions and epileptiform fits occuring particularly in heavy infestation 9. Vomiting may occur if the worm is abnormally present in the stomach. 10. It is usual to observe flea and or flea debris on skin of dog or cat infested by Dipylidium caninum. 11. Progressive emaciation due to flea bite as well as animals were off food.
12 4/6/2017
Dipylidium caninum
PM Diagnosis • Enteritis • Visual detection of gravid segment in • Presence of tape worm (segmented 1/2 – stool 1 m) • Microscopic examination of gravid segment for demonstration of the egg nest or the egg packet. • Direct fecal exam • Concentration floatation technique.
13 4/6/2017
Dipylidium caninum Egg Nest
14 4/6/2017
Dipylidium caninum
Treatment: • Anthelmintics for tapeworms infestations are Praziquantel compound (Distocide®) which is the drug of choice. • Not every drug that affects ascaris affects dipylidium)
Control: • Eradication of flea from the place • Eradication of flea from the animal => revolution (cat) or diazenone (dog) or shampoo or Bars
Public Health Importance: • Accidental ingestion of flea
BABESIOSIS
15 4/6/2017
A tick transmitted disease characterized by high fever, red urine, jaundice and invasion and destruction of RBCs and acute hemolytic anemia
• Etiology: 1- B. Canis (large babesia) 2- B. gibsoni (small babesia)
• Inefctive Stage: Sporozoits
16 4/6/2017
Life cycle and epidemiology
•Brown dog tick (Rhipicephalus sanguuineus and Haylomma species) •Infected blood transfusions. •Ticks acquire the infection by ingestion of blood from infected dogs. •Babesia reproduces sexually and asexually in ticks and there is trans-ovarian transmission. •The clinical disease is sporadic and its severity relate to age and immune status of the host. Young dogs are particularly susceptible.
Clinical signs
• Sub clinical and carrier dogs are common
• There are 3 forms of the disease: 1. Per acute,
2. Acute and
3. Chronic
17 4/6/2017
Clinical signs
1- Peracute form
• Sudden onset, shock and rapid death
Clinical signs
2- Acute Form • High fever 41 °C, Anorexia, depressed. • Vomiting • Mucus membrane becomes congested (at fever stage) then pale and anaemic (destructed RBCs) then icteric with Jaundice and • Red urine • Enlargement of lymph nodes and spleen "Spleenomegaly" with oedema of the head and neck and petechiae of the mucous membranes may be observed. Severely affected animals develop shock and die. • Regenerative anaemia because the body sends immature RBCs into circulation to make up for those that are lost to the disease
18 4/6/2017
Clinical signs
3- Chronic Form • Anemia • Intermittent fever • Loss of condition
19 4/6/2017
20 4/6/2017
urinary bladder contains dark red urine due to hemoglobinuria (red water)
Differential Diagnosis
• The disease should be differentiated from diseases causing intravascular haemolysis such as: 1. Bacterial toxins including leptospirosis 2. Acute autoimmune anaemia 3. Zinc toxicity 4. Blood transfusion reactions 5. Snake venom
21 4/6/2017
Diagnosis
1. Demonstration of Babesia as pyriform organisms in red cells in Giemsa – stained blood smear. Blood collected from the ear vein is preferred. 2. Serological test : indirect fluorscent test is commonly used (IFT). 3. A regenerative haemolytic anaemia is present. 4. Bilirubinaemia, bilirubinuria, hemoglobinuria and acidosis is usually present. 5. PCR
22 4/6/2017
Treatment
1. Dogs that have improved on their own may relapse with stress and exertion 2. Single treatment with diminazene aceturate (3.5mg/kg IM) (berenil) or Imidocarb diproprionate (5mg/kg deep IM) (imizol) 3. Fluid therapy to correct acidosis and shock . 4. Vitamin B complex should be given in severe anaemia. 5. Collars that contain amitraz (Preventic Collars) combined with monthly fipronil spray (Frontline Plus) or Revolution (Selamectin) drops are quite effective in repelling ticks
DON’T FORGET THE VECTOR ”TICKS”
Control
1. Routine dipping of animals and spraying of premises with acaracides (Diazinon or butox). 2. Shampoos and dips that kill and repel ticks 3. Treat your yard with insecticides approved for controlling ticks 4. Care during blood transfusion
23 4/6/2017
CANINE EHRLICHIOSIS
Etiology
• It is a generalized disease caused by the rickettsial organism Ehrlichia canis.
• Ehrlichia canis is an obligate intracellular pathogen of monocytes and lymphocytes.
• It is widely distributed especially in the middle east, Africa , India and the USA.
24 4/6/2017
Epidemiology
Mode of Transmission and infection:
• The brown tick , Rhipicephalus sanguineus is the primary vector
• This 3-host tick is capable for transmission of the organism for 5 months after engorgement
• Blood transfusion or other means by which infected WBC are transferred, also transmit the disease.
Epidemiology
Pathogenesis and pathology: • Replication of the organism occurs in the mononuclear cells with haematogenous spread resulting in splenomegaly, hepatomegaly and lymphadenopathy.
• Vasculitis, thrombocytopenia, anemia and leukopenia are observed in the acute stage of the disease.
• Progression from the acute to chronic stage, depends on the strain of the organism and immune status of the host.
• Dogs can remain carrier s for more than 2 years after recovery from the acute form and acts as a long –term reservoir of the organism.
25 4/6/2017
Clinical signs
• IP ranges from 8-20 days Acute form :- 1. lasting from 2-4 weeks. 2. Fever, anorexia, weight loss, enlargement of the superficial lymph nodes. 3. Stiffness, oedema of the limbs or scrotum and coughing or dyspnea. 4. Recovery may occur in some dogs or progress to the chronic form.
In the chronic form : - 1. 50% of affected dogs show petechiae and ecchymoses on the abdomen and M.M. 2. Epistaxis, haematuria and melena are common. 3. Anterior uveitis, retinal detachment with corneal oedema and blindness. 4. Nervous signs as cerebellar ataxia, paresis and hyperaesthesia may be present. 5. Severe weight loss is a prominent finding.
Anterior uveitis
26 4/6/2017
Diagnosis
1. Demonstration of the organism with in WBCs in blood smear or buffy coat layer using Giemsa stain. 2. IFAT is sensitive and specific 3. Haematological findings include thrombocytopenia, anemia and leukopenia 4. Abnormal biochemical findings which include hypergammaglobulinaemia.
Erlichia canis or Canine monocytic ehrlichiosis (CME)
27 4/6/2017
Differential diagnosis
• In the acute stage, must be differentiated from 1. Brucellosis, 2. Blastomycosis, 3. Immune-mediated disease, and 4. Systemic lupus erythromatosus.
• In the chronic form: must be differentiated from 1. Babesiaosis. 2. Estrogen toxicity, 3. Glomuleronephritis and 4. Immune-mediated pancytopenia.
Control and Treatment
1. Doxycycline (5-10mg/kg orally at 12 hours intervals for 10 days) is the drug of choice. 2. Oxytetracycline (22 mg/kg orally, 3 times daily for 2 weeks) is effective. 3. Fluid therapy, blood transfusion and vitamin supplementation are necessary. 4. Acaricides for tick control. 5. Tetracycline (6.6mg/kg per os daily) can be used prophylactically for susceptible dogs in endemic areas.
28 4/6/2017
TOXOPLASMOSIS
Toxoplasmosis
Toxoplasmosis is one of the most common parasitic diseases of warm-blooded animals, including pets and humans
29 4/6/2017
Toxoplasmosis
• Etiology: • Final Host: Toxoplasma gondii Felines (wild and domestic) • MOI: • IMH: • In cats: Warm blooded animals 1. Direct contact with infected soil • Infective Stage: 2. Ingesting infected rodents, birds, raw Sporulated oocyst meat • In Human: 1. Foodborne (ingesting contaminated food) 2. Animal-to-human (ingestion of sporulated oocyst) 3. Mother-to-child (congenital)
Epidemiology
• Three forms of T. gondii can initiate infection in cats or other vertebrates:- 1- The tachyzoite which is the actively proliferating form seen in disseminated infection and present in blood, urine, saliva, semen and faeces. (Crescent – shaped).
2- The bradyzoites or the resting form and is present in congenital, acquired or a symptomatic infection. It is found in cysts mainly in the liver, brain, eye and skeletal and cardiac muscles. It is destroyed by cooking to 66°C.
3- The oocyst which passed in the faeces of susceptible cats following ingestion of any of the 3 forms.
30 4/6/2017
Life Cycle Cat ingests infected prey (or infected meat) ↓ Parasite is released into the cat's digestive tract, multiply in the wall of the small intestine and produce oocysts during what is known as the intra-intestinal infection cycle ↓ Oocysts are excreted in feces (start 3-5 days after infection and may continue up to 3-20 days) ↓ Oocysts are very resistant and may survive in the environment for well over a year ↓ During the intra-intestinal infection cycle, some organisms are released from the ingested cysts, penetrate more deeply into the wall of the intestine and multiply as tachyzoites ↓ Tachyzoites then spread out from the intestine to other parts of the body, starting the extra-intestinal infection cycle ↓ Immune system restrains this stage, which enters resting stage by forming cysts in muscles and brain ↓ These cysts contain bradyzoites, (slowly multiplying organisms)
31 4/6/2017
Toxoplasma oocyst (Sporulated)
Toxoplasma gondii (Tachyzoite)
32 4/6/2017
Toxoplasma gondii (Bradyzoite)
Clinical signs
• Most cats are a symptomatic • Signs are most severe in cats under 1 year of age especially young kittens • Fever, lethargy, anorexia and dyspnea due to pneumonia are the most frequent signs of generalized infection. • Gastro-intestinal or hepatic signs such as icterus, vomiting and diarrhea and abdominal effusion may occur. • Nervous manifestations in the form of encephalitis, myeilitis and peripheral myopathy or myositis appears as incoordination, circling, head pressing, difficulty in chewing and swallowing food, seizures and loss of control over urination and defecation. • Weakness with hyperaesthesia on muscle palpation or shifting leg lameness. • Ocular lesions in the form of unilateral or bilateral uveitis and retinal hemorrhage leads to blindness
33 4/6/2017
Diagnosis
1. Case history 2. Isolation of T. gondii by I/P inoculation of suspected material into mice free from natural infection. Mice died after 5-12 days and giemsa stained smears of peritoneal exudates show many intracellular and free forms of the parasite. 3. Serological test for the detection of antibodies which include indirect immunofluorscence, indirect haemagglutination and ELISA. IgM titres > 1:64 and four fold increase in IgG 4. Significant IgG antibodies suggests end of infection or previous infection 5. Significant IgM antibodies suggests an active infection or clinical Toxoplasmosis. 6. Microscopic examination of tissues or tissue impression smears for distinctive pathologic changes and the presence of tachyzoites 7. PCR
• Treatment: 1. Clindamycin (5-20mg/kg IM every 12 hours for 3 months) 2. Pyrimethamine and sulfadiazine (inhibit T. gondii reproduction)
• Prevention and Control: 1. Do not eat raw or undercooked meat or drink unpasteurized milk 2. Wash hands, utensils and surfaces with warm soapy water after handling raw meat 3. Control rodents 4. No vaccine is available
• Public Health Importance: Accidental ingestion of oocysts (after cleaning the litter box, from contaminated soil, drinking contaminated water) Pregnant women can pass the infection to their unborn child (congenital infection)
34 4/6/2017
TICK INFESTATION
Rhipicephalus sanguineous tick Three host tick, Kennel tick, Pan tropical dog tick
About 3200 egg
35 4/6/2017
36 4/6/2017
MANGE
37 4/6/2017
Types of Mange
1- Sarcoptic mange: • Causes hair loss and crusty skin (uncommon in cats) 2- Otodectic mange: • Another name for ear mites 3- Demodectic mange: • Causes hair loss and inflamed skin • It may be localized, with small amounts of hair loss and discrete patches of red, inflamed skin • Or general in nature in several spots on the body • Uncommon and depends on immune system
DEMODICOSIS (FOLLICULAR MANGE OR RED MANGE OR DEMODECTIC MANGE DEMODECTIC ACARIASIS)
38 4/6/2017
It is a parasitic dermatitis, with varying degree of pruritus resulting from proliferation of the follicular mange mites. It is a disease of dog and cat caused by Demodex canis (dog) and Demodex cati (cat) characterized clinically by alopecia, itching and it usually occurs in immune suppressed animals.
Life Cycle (18-24 days)
Demodex is a normal inhabitant on the animal skin ↓ Female lays 20-24 eggs ↓ Eggs hatch to give larvae ↓ Larvae and nymph mature within the hair follicle
39 4/6/2017
Epidemiology
Mode of transmission: • By direct contact with all stages of Demodex spp.
Mode of Infection: • Direct contact
Infective Stage: • All stages (egg-larva-nymph-adult)
Susceptibility: • 3-12 months of for canine demodecosis. • The demodecosis is more common in dogs (German Shepherd Dog) than in cats. • Immunosuppression plays very important role in the development of Demodecosis.
Clinical signs
Localized Form (Juvenile demodecosis) 1. Mild benign self-limiting disease, is very common in dogs 3-12 months of age
2. Lesions mainly around the muzzle, eyes or mouth and limbs
3. Appear as patches of partial alopecia sometimes with Erythema and scaling
4. No itching
5. Most infected animals are spontaneously recovered and only 10% of untreated ones progress to the generalized form.
40 4/6/2017
Clinical signs
Generalized Form 1. Generalize serious and potentially life-threatening disease usually seen in immune suppressed animals due to concurrent diseases or prolonged immune suppressive therapy. 2. In both young and adult 3. Painful lesions usually occur on the head, neck, legs and trunk with alopacia, erythema, pyoderma and seborrhea with a characteristic bad odour. 4. There is no itching except when there is secondary bacterial infection. 5. Peripheral lymphadenopathy. 6. The severe cases are characterized by wide skin disfigurement, lethargy, inappetance and septicaemia and death. 7. Demodectic pododermatitis is a chronic digital and inter-digital disease with pyoderma may appear in some cases.
Demodicosis
41 4/6/2017
Peri-ocular demodicosis
A) Adult Demodex mite. B) Demodex egg
42 4/6/2017
43 4/6/2017
Diagnosis
• Skin scraping: deep skin scrap with tap water (or diluted NaOH 1:10) and examined under microscope
Control and Treatment
1. Localized demodecosis is spontaneously regressed. 2. Correct predisposing factors such as immune suppression and concurrent diseases. 3. Amitraz®(1% solution) or rotenone are the acaricides of choice and treatment should be continued untill the dog is clinically normal and skin scraping is negative 4. Dectomax® 5. Revolution® 6. Increase immunity by using Non-specific immunostimulants e.g levamizole. 7. Hair growth treatment 8. Vitamin 9. Antibiotics in cases of secondary infection 10. Isolation 11. Treatment of concurrent diseases and avoid prolonged immune suppressive therapy. 12. No over crowding 13. Disinfection of the area (OPC)
44 4/6/2017
45