A. According to etiology: 1. Bacterial. 2. Viral 3. Parasitic 4. mycotic

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1 Infectious disease: it is any disease caused by pathogenic agen (bacteria, virus, parasite), must be invade tissue of susceptible animal and multiply inside tissue. Calssification of infectious diseases: A. According to etiology: 1. Bacterial. 2. Viral 3. Parasitic 4. mycotic

2 A. According to course: 1. Acute (1-2 w) 2. Subacute ( few weeks) 3. chronic (months or years) B. Acccording to transmissability: 1. Contagious disease: the disease transmitted from reservoir to susceptible host either direct or indirect. 2. Infectious disease C. According to occurance: 1. Exotic disease, the disease enter the countery for first time. 2. Sporadic disease, the disease appear in individual cases. 3. Endemic disease the disease appear in regularity in population. 4. Epidemic disease, the disease occurs in level exceed than expected level.

3 Mode of transmission: It is the mean of transmission of the disease from infected to susceptible animal. Horizontal transmission, it is transmission of the disease from segment of population to another directly or indirectly. Direct transmission: the susceptible animal contact with infected one (as touch, a scratch) or contact at distance (dropplet infection) Indirect transmission, the disease transmitted mechanical, biological as ticks, mosquito or inanimate objects as vehicles or biological product. Vertical transmission, it is transmission of the disease from animal of one generation to subsequent generation (transplacental, transovarian, transmammary)

4 Disease 1. Definition 2. Etiology 3. Epidemiology 1. Distribution 2. Animal susceptibility 3. Mode of transmission Pathogenesis Clinical signs PM Diagnosis Field diagnosis Lab diagnosis Treatment control

5 STRANGLES Infectious adenitis or distemper

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7 Definition It is an acute infectious disease of equine (mainly young horses) which caused by streptococcus equi and characterized by inflammation of the upper respiratory tract, pyrexia, anorexia and abscessation of the regional lymph nodes particularly submaxillary and pharyngeal lymph nodes.

8 Etiology Streptococcus equi subsp. equi (S. equi) is a Grampositive, non motile and non spore forming, coccobacillus, arranged in pairs or chains that produces a betahemolysin, evident as a zone of clear hemolysis surrounding colonies growing on blood agar. The organism identified serologically according to lancefield serologic grouping on basis of cell wall polysaccharides into Strpt. equi lancefield group C. it avoids destruction by neutriphiles through several virulence factors as capsule, antiphagocytic M-proteins and leukocidal toxins

9 Predisposing factors: Age, young age animals are commonly infected due to local immunity are low but adult can infect if it not infect on young age. Debility, fatigue and transportation. Malnutrition and bad hygiene. Strangles occurs more commonly among stable animals than outdoors animals. Strangles usually appears after a period of cold rain, or when there had been a hot or dry wind. Concurrent infections as Parainfulenza and debilitating disease

10 Epidemiology Distribution: It is worldwide distributed and endemic in Egypt. Animal susceptibility: horses, donkeys, asses and mules of any age but young one are more affected of 6 m to 2 y. and rarely over 5 y. Transmission: Source of infection: Nasal, saliva and abscess discharge from infected animals Approximately 10-40% of horses that recover from the clinical disease has persistent infection of S. equi in the pharynx and guttural pouches for many months and are an important source of infection Mode of infection: It is transmitted by direct contact with infected animals (nose to nose or nose to mouth) or indirectly through contaminated fomites (contaminated food, water and utensils). Infection occurs through inhalation of infected droplets or ingestion of contaminated food and water.

11 Pathogenesis Following exposure of the oral and nasopharyngeal mucosal surfaces to S. equi, bacteria lodge in the pharyngeal and tonsillar lymphoid tissues where they multiply rapidly. There is no evidence of colonization of mucosal surfaces, The binding of S. equi to pharyngeal cells is caused by fibrinogen binding proteins associated with M protein. The resistance of S. equi to non-immune phagocytosis results in accumulation of large numbers of organisms surrounded by degenerating neutrophils. Release of streptolysin S and streptokinase may contribute to tissue damage by directly injuring cell membranes and indirectly through activation of plasminogen, Bacteremia may occur

12 Migration of neutrophils into the lymph nodes causes swelling and abscessation Swelling of retropharyngeal lymph nodes may interfere with deglutition and respiration Nasal shedding of S. equi usually begins 4-7 days after infection, or 2 days after onset of fever, and persists for 2-3 weeks in most horses but up to years in exceptional horses Death is usually due to pneumonia caused by aspiration of infected material, although other causes of death include asphyxiation secondary to upper airway swelling and impairment of organ function by metastatic infection Metastatic infection of the heart valves, brain, eyes, joints, and tendon sheaths or other vital organs may occur and cause a chronic illness and eventual death.

13 Clinical signs IP is 4-8 d, morbidity rate is varying according to age, 10-50% and may reach to 80%, mortality rate is low 3% and course of the disease is 2-4 w. Acute form: Diphasic fever ( C), subside after 2-3 d and raise again when abscess in the lymph node are developed Nasal discharge, bilateral a serous nasal discharge, which rapidly becomes copious and purulent, and a severe pharyngitis and laryngitis. Rarely there is a mild conjunctivitis. Lymphadenopathy becomes apparent as the submandibular lymph nodes enlarge and palpation elicits a painful response. The pharyngitis may be so severe that the animal is unable to swallow and there is a soft, moist cough. The head may be extended. Swelling of the retropharyngeal lymph nodes may cause obstruction of the oro- and nasopharynx with subsequent respiratory distress and dysphagia. Death by asphyxiation may occur at this time in severe cases. Obvious swelling of the nodes may take 3-4 days to develop; the glands begin to exude serum through the overlying skin at about 10 days and rupture to discharge thick, cream-yellow pus.

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15 Bastard form: Formation of abscess in any organ or body site but most commonly in the lungs, mesenteric lymph nodes, liver, spleen, kidneys, and brain. Clinical signs depend on the organ affected and the severity of the infection, but intermittent fever, chronic weight loss and sudden death due to rupture of abscesses into a body cavity are common manifestations of metastatic infection. Metastatic infections may occur in the central nervous system. Extension of infection to the meninges results in suppurative meningitis characterized clinically by excitation, hyperesthesia, rigidity of the neck, and terminal paralysis. Abscesses in the brain cause a variety of clinical signs, depending on location of the abscess, including severe depression, head pressing, abnormal gait, circling, and seizures, Metastatic infections of the ocular and extraocular structures, heart valve s and myocardium, joints, bones, tendon sheaths, and veins may occur.

16 Atypical or mild form: It is characterized by widespread subclinical infection and a mild disease. Affected horses have a transient fever for hours and a profuse nasal discharge, and are anorexic. A moderate enlargement of the mandibular lymph nodes occurs in only about one-half of the affected horses.

17 Complication: It occurs in about 20% of infected animals. Several immune-mediated conditions are: Purpura hemorrhagica: as a result of antigen-antibody complexes which causing vasculitis resulting in edema and petichation and serum exudation with signs of S/C swelling, mucosal hemorrhage and fever. This may follow acute disease in about 3 w and occurs commonly in animals previously infected or vaccinated against strangles. Post strangles myocarditis: due to antibody at M. protein react with heart myosin. Post strangles anemia due to antigen-antibody complexes attaches to erythrocyte and removal of theses from circulation by reticuloendothelium system. Guttural pouch emyemea and sinusitis with dysphagia and laryngeal hemiplegia.

18 Postmortem lesions: Extensive suppuration in lymph nodes and internal organs particularly liver, spleen, lungs, pleura and peritoneum

19 Diagnosis Field Diagnosis: It is based on contagious nature of the disease among young horses and clinical signs of fever, lymphadenopathy of the throat lymph nodes with nasal discharges.

20 Laboratory diagnosis: Samples: Nasal discharge, pus, nasal swabs, blood and paired serum samples. Laboratory examinations: Direct microscopic examination of stained smear, the organism is Gram positive cocci exist in pair shapes. Isolation of organism on blood agar, and identification of the colony by staining or biochemical reaction. Serological examination as passive hemagglutination test. Animal inoculation as mice, pus inoculation will kill it in 2-4 days with evidence of acute septicemia.

21 Treatment Isolation of infected animal and treat as soon as possible as following: Medical treatment: specific treatment is pencillin, first dose begine a combination of crystalline and procaine pencillin of 200 and 500 IU/kg BW respectively. The second dose is procaine pencillin alone at 24 h intervals for 3-5 d. Cases with purpura hemorrhagica should be treated by antiinflammatory, antihistaminic, calcium therapy, diuretics and blood transfusion. Surgical treatment: Iodine or icthyol ointment locally on enlarged nodes or hot fomentation to ripen the abscess with daily surgical dressing of the abscess after pus evacuation. Tracheotomy if there is dyspnea or compression on pharynx. Hygienic treatment: rest of infected animal, provide soft palatable diet, clean separate water and food bucket and keep nostrils and muzzles clean with frequent removal of discharges and washing with antiseptic.

22 Control Proper management: Affected horse should be isolated for at least 6 weeks with strict hygiene control of all in contact workers and utensils. The contact of the healthy animals with contaminated food, water, infected premises should be avoided. Stalls and stable requirements such as pails, brooms, grooming brushes and blankets should be cleaned and disinfected and the bedding should be burned. New introduction, particularly yearling horses should be isolated for 2-3 weeks before their introduction to the herd. Vaccination: Horses can be vaccinated with Strep. equi bacterin (Equibac II) and recently by M-protein extract vaccines (strepvax). Vaccination is usually carried out in young foals at 12 weeks of age. It is carried out by 3 successive doses at 3 weeks are recommended. Passive immunity from the immunized dams provides protection for foals in the early life till weaning.