Anti Parasitic & Anti-protozoal drugs

Introduction:

➡️Term ‘strangles’ derives from enlarged retropharyngeal lymph nodes and guttural pouches causing respiratory distress in severely affected horses.

➡️It is an acute highly contagious bacterial disease of horses characterized by inflammation of the upper respiratory tract and also abscess formation in the regional lymph nodes.

➡️Strangle affect horses of all ages but mostly occurs in young horses.

➡️It occurs in horses, ponies, donkeys and mules worldwide except Iceland.

➡️This disease is important not only because of death rate but because of esthetic unpleasantness due to running noses and abscesses.

➡️Most cases recover quickly unless the enlarging lymph nodes obstruct the upper respiratory tract

Etiology:

➡️Causative agent- Streptococcus equi subsp.equi or Streptococcus equi

➡️Family – Streptococcaceae

➡️Phylum- Firmicutes

➡️Order – Lactobacillales

➡️Genus- Sterptococcus

➡️S.equi is a gram positive cocci bacteria and grow in pair or chain form

➡️According to Lancefield classification S.equi classified under group C and closely related to S. equi ssp. zooepidemicus.

➡️S. equi ssp. zooepidemicus infect a variety of species but  S. equi spp. equi  infects  only horses.

Virulence factors:

➡️Hyaluronic acid capsule - Mediates binding of bacterium to host cells

                                                    -Resistance to phagocytosis

 

➡️M protein and Factor-H–binding protein –It bind to fibrinogen and prevent deposition of C3b by this action it block recognition and phagocytosis by macrophages.

Source of infection:

➡️Organism live prolonged as carrier state in asymptomatic animals

➡️Direct transmission – Contact with infected animals

➡️Contaminated fomites - contaminates pasture, tack, stalls, feed and water troughs etc.

➡️Nasal and abscess discharges

➡️Even veterinarian may also source of infection

➡️Organisms survive in the environment for less than 3 days but in exudates they can survive for many months

Pathogenesis:

➡️Pathogenesis of strangle is depend on virulent factors

M  protein :

➡️M surface protein of S. equi help to organisms in adhesion to oral, nasal, and pharyngeal tissues and also invasion of pharyngeal tonsils and regional lymphoid tissues.

➡️furthermore  it also associated with evasion  of the innate host immune response or protect organism against innate immune response

➡️Two types :  (1)SeM

                     (2) SzPSe

 

➡️SeM is unique and plays a role in protect the organism to phagocytosis

➡️These  proteins interfere deposition of C3b on the surface of the bacteria and bind to fibrinogen.

➡️In short,it reduce susceptibility of the S.equi to phagocytosis by neutrophils. 

Hyaluronic acid capsule:

➡️It protect S.equi against nonimmune phagocytosis and has role in pathogenicity.

➡️If Strains of S. equi that do not have  a capsule then they do not produce disease.

Pathogenesis

Oral and nasopharyngeal mucosal surfaces get exposure of  S. equi organism

↓ 

 Bacteria lodge in the pharyngeal and tonsillar lymphoid tissues and multiply

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S.equi  bind to pharyngeal cells through fibrinogen binding proteins associated with M protein and become resistant to non immune phagocytosis

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Accumulation of large numbers of bacteria that surrounded by degenerating neutrophils

 ↓ 

S.equi release  streptolysin and streptokinase that may contribute to tissue damage  by directly injuring cell membranes and indirectly by activation of plasminogen

 ↓ 

Bacteremia may occur

 ↓ 

Neutrophils migrate into the lymph nodes and causes swelling and abscessation  ( 48 hours )

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 Cause disruption of lymph drainage and development of edema in tissues which drained by the affected nodes

 ↓ 

Swelling of retropharyngeal lymph nodes may interfere with deglutition and respiration, in severity of swelling of this lymph node may cause death due to asphyxia

 ↓ 

Most abscess rupture and drain

 ↓ 

 Infection resolves with development of an effective immune response

➡️4 to 7 days after infection- nasal shedding of S. equi

➡️2 days after - onset of fever

➡️Persists for 2 to 3 weeks in most of  horses but in exceptional cases up to years

Clinical Signs:

Acute infection:

➡️Mucopurulent nasal discharge

➡️Abscessation of sub mandibular and retro pharyngeal lymph nodes

➡️Complete anorexia,

➡️Depression,

➡️Fever  (103–105° F),

➡️Serous nasal discharge becomes copious and purulent

➡️Severe pharyngitis and laryngitis.

➡️Sub-mandibular lymph nodes enlarge and on  palpation elicits a painful response

➡️Swelling of retropharyngeal lymph nodes cause obstruction of the  nasopharynx - respiratory distress

➡️Death by asphyxiation in severe cases

➡️Abscess rupture to discharge thick, cream-yellow pus

➡️Retro pharyngeal abscesses can rupture into the guttural pouches- cause guttural pouch emphysema

➡️Infection can spread to local lymphatic vessels causing obstructive edema – mostly in lower

Sub-clinical infection:

➡️Transient

➡️Fever for 24 to 48 hours

➡️Profuse nasal discharge

➡️Anorexia

➡️Moderately enlargement of the mandibular lymph nodes

➡️Strangles in burros is a slowly developing debilitating disease

➡️At PM examination - caseation and calcification of abdominal lymph nodes

➡️Chronic disease associated with metastatic infection of organs away from upper respiratory tract.

Macroscopic Pathology:

➡️Suppuration in internal organs especially liver, spleen, lung etc.

➡️Submandibular and retropharyngeal nodes are first most severely affected

➡️Initially, swollen lymph nodes are firm, but  swelling becomes fluctuant as suppurative exudates with time

➡️Most favorable clinical outcome -  lymphadenitis with rupture of abscesses onto the skin at 1-3 weeks after onset of infection

➡️Creamy yellow-white pus containing numerous infective bacteria

➡️Purulent exudates find into guttural pouch in complicated cases

➡️Drainage from the guttural pouch into the nasal cavity is a major reason for suppurative nasal discharge

➡️Retropharyngeal abscesses may discharge into the pharynx and  pus to be aspirated into lungs-  causing necrotizing pneumonia in localized area

➡️Metastatic abscesses or bastard strangles- occasionally form in the liver, kidneys, synovial and brain but are mostly in mediastinal and mesenteric lymph nodes

➡️Purpura hemorrhagica develops in 1-2% of cases at 2-4 weeks after the acute infection

Diagnosis:

➡️Based on history and clinical signs

 

➡️SAMPLE – nasopharyngeal swabs

discharges from abscesses

guttural pouch lavage

 

➡️Confirmation diagnosis -  Culture  S. equi on selective media

Beta hemolytic dew drop like colony on blood agar

 

➡️Serologic tests to measure antibodies to SeM

➡️ELISA

➡️PCR 

Treatment:

➡️Choice of treatment- penicillin

➡️Procaine penicillin G - 22,000 IU/kg IM b.i.d

                    or

➡️Potassium or sodium penicillin G - 22,000 IU/kg IV every 6 hours

➡️Tetracycline- 6.6 mg/kg IV every 12-24 hours and sulfonamide–trimethoprim combinations (15-30 mg/kg orally or IV b.i.d) can be efficacious but should only be used if penicillin cannot be administered

References:

Pathologic Basis of Veterinary Disease Expert Consult

6th edition

By: James Zachary, M. McGavin