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