Strangles Flashcards
What are the initial signs of the disease in horses?
Abrupt pyrexia (sudden onset of fever), pharyngitis (inflammation of the pharynx), and abscess formation commonly in submandibular and retropharyngeal lymph nodes.
Which age group of horses is most susceptible to the disease?
Horses aged 6-10 years are most commonly affected based on surveillance via qPCR.
How does the disease severity vary with the age of the horse?
Younger horses exhibit more severe signs, while older horses are less affected and recover faster.
What factors influence the variability in the presentation of the disease?
The immune status of the horse and the fact that not all horses show classic signs.
When do the first signs of the disease typically appear post-exposure?
First signs usually include fever and lethargy occurring 3-14 days post-exposure.
How severe can the fever get in horses with this disease?
Fever can be severe, exceeding 42°C (107.6°F), and may persist until abscess rupture.
What are the accompanying symptoms of significant pharyngitis in horses?
Reluctance to eat or drink, abnormal head positions due to pain, nasal discharge, and a soft, mucoid cough often associated with eating.
What signs indicate laryngeal pain in horses?
Pain on squeezing the larynx causing stridor, gagging, and coughing.
Which lymph nodes are commonly affected by the disease?
Submandibular and retropharyngeal lymph nodes, occasionally parotid and cranial cervical.
Describe the development and rupture of abscesses in horses.
Abscesses develop a thick fibrous capsule and rupture in 7 days to 4 weeks. Initial signs include warm, diffuse swelling, serum oozing from the skin before rupture, and thick purulent discharge either externally or internally.
What are the signs of empyema of the guttural pouch in horses?
Expulsion of discharge with coughing or eating, and intermittent unilateral nasal discharge and cough in approximately 50% of cases.
What neurological impacts can occur due to this disease?
Neuropraxia causing temporary laryngeal hemiplegia or dysphagia, damage to the recurrent laryngeal nerve, paralysis of arytenoid cartilage, and dysphagia with potential reflux of feed or water from nares.
What is “bastard strangles” and what sites can it affect?
Abscesses in multiple sites including the brain, abdomen, and mammary gland; it is a term used for metastatic abscesses.
How does S. equi enter and attach to the host cells?
S. equi enters through the mouth or nose, attaching to cells within the crypts of the lingual and palatine tonsils and the follicular-associated epithelium of the pharyngeal and tubal tonsils. Initial binding is facilitated by exposed surface proteins such as SzPSe.
What happens within a few hours after S. equi penetrates the host cells?
The organism penetrates and becomes difficult to detect on the mucosal surface but is visible within epithelial cells and subepithelial tonsillar follicles. Note that nasal or NP samples may be culture negative in the early stages of infection.
What occurs during the early stages of S. equi infection?
Translocation to mandibular and retropharyngeal lymph nodes occurs within hours, involving complement-derived chemotactic factors attracting polymorphonuclear neutrophils. Abscess formation is not grossly evident for 3-5 days post-infection.
What mechanisms does S. equi use to evade phagocytosis?
Neutrophils fail to phagocytose and kill S. equi due to hyaluronic acid capsule, antiphagocytic SeM protein, H factor binding Se18.9, Mac protein, and other undetermined factors.
How is effective bacterial disposal achieved in S. equi infection?
Effective bacterial disposal relies on the lysis of the abscess capsule and evacuation of its contents.
When does nasal shedding of S. equi begin and how long does it last?
Nasal shedding begins 2-3 days after fever onset, lasting 2-3 weeks in most horses. Some horses with preexisting immunity may not exhibit detectable shedding, and persistent shedding can occur if infection persists in the guttural pouch or sinus.
What are the characteristics of immune responses to S. equi infection?
Systemic and mucosal immune responses develop 2-3 weeks post-infection, coinciding with mucosal clearance. Natural exposure and infection boost immunity and contribute to herd immunity, with 75% of horses developing long-term immunity without antibiotic treatment.
What is the infectious dose of S. equi in natural transmission?
The infectious dose in natural transmission is lower than in propagated media, as virulence factors are better expressed in vivo. Inocula of less than 10^6 colony-forming units are often insufficient to cause disease due to effective mucociliary clearance.
What is convalescent immunity and how effective is it in horses recovering from S. equi infection?
Horses develop resistance to high experimental challenges during the convalescent phase. However, 20-25% may be susceptible to reinfection within months, indicating inadequate mucosal and systemic antibody maintenance. Approximately 75% develop long-term immunity.
What are catarrhal or atypical strangles, and how do they affect horses?
Older horses with residual immunity, foals with waning maternal antibodies, and vaccinated horses exhibit milder forms of strangles but still shed virulent S. equi. These horses still shed virulent S. equi and can induce severe disease in naïve individuals.
How do mares provide passive immunity to their foals?
Milk from mares recovering from strangles contains IgGb and IgA, providing passive immunity to suckling foals. Colostral antibodies ingested in the first 24 hours recirculate to the nasopharyngeal mucosa, offering additional protection.
What is the timing of shedding for S. equi and its implications for isolation?
Shedding typically starts 1-2 days after fever onset, allowing potential isolation before transmission. Nasal shedding lasts 2-3 weeks, with infectious potential up to 6 weeks after discharges cease. Persistent guttural pouch infections may shed intermittently for years.
How is the severity of S. equi disease linked to infectious exposure?
The severity of the disease is linked to the dose and frequency of infectious exposure.
What are the primary sources of S. equi infections in active and recovering horses?
Horses with active or recovering strangles due to purulent discharges from lymph nodes, nose, and eyes.
How does direct transmission of S. equi occur?
Through direct horse-to-horse contact and normal equine social behaviors such as head-to-head or nose-to-nose interactions.
What are some methods of indirect transmission of S. equi?
Sharing contaminated housing, water sources, feed, or feeding utensils, and the use of shared twitches, tack, and other equipment. Less obvious fomites like the clothing and equipment of handlers and veterinarians can also be sources. Anecdotal evidence suggests transmission via other animal species is possible.
Why are healthy carriers significant in the spread of S. equi?
Healthy-appearing animals can significantly spread S. equi, especially in initiating new outbreaks or recurrences in previously affected herds.
What is the role of horses incubating S. equi disease in transmission?
Some horses that are incubating the disease may appear outwardly healthy and infectious. These horses eventually develop signs of strangles, and their nasal secretions are assumed to be the source of infection.
What defines convalescent carriers of S. equi?
Outwardly healthy horses that have fully recovered may continue to harbor the organism. These horses can remain infectious for at least 6 weeks after purulent discharges have dried up. Periodic shedding of S. equi can occur for prolonged periods after apparent full recovery. These horses are referred to as long-term, subclinical carriers and can be a source of new or recurrent disease in well-managed groups of horses.
How long can recovered horses remain infectious after purulent discharge clearance?
Recovered horses can be infectious for at least 6 weeks post-discharge clearance.
What is necessary for the effective control of long-term carriers?
Detection, segregation, and treatment of these carrier animals.
What characterizes most outbreaks of S. equi?
Most outbreaks are highly clonal, indicating transmission from a single source. Both active and persistent carriage strains can be identified in chondroids (hardened pus) from horses in the same stable. Genomic analysis of isolates from various large outbreaks shows evidence for the persistence of S. equi, leading to new clinical cases.
How long can S. equi remain viable in water?
S. equi remains viable in water for 4-6 weeks.
How does S. equi survive in feces or soil under real-world conditions?
It does not survive well in feces or soil under real-world conditions.
What is the observed survival time of S. equi on fencing and soil?
Rapid death (1-3 days) on fencing and soil when in direct sunlight observed in recent studies.
What environmental factors affect the survival of S. equi?
S. equi is sensitive to bacteriocins from environmental bacteria and does not survive well in the presence of other soil-borne flora.
What is the optimal sample for confirming S. equi infection?
A needle aspirate from an enlarged or abscessed lymph node.
How effective are nasopharyngeal swabs for detecting S. equi?
Nasopharyngeal swabs are useful but may miss early infection due to rapid bacterial invasion of lymph nodes and intermittent shedding.
Why are nasopharyngeal and guttural pouch washes preferred?
They are more sensitive than swabs, especially in detecting persistent infections, and are indicated for subclinical carriers.
Describe the procedure for nasopharyngeal washes.
Instil 50 mL of warm normal saline via soft latex tubing or uterine pipette to the level of the nasal canthus, collect the washings into a disposable cup or rectal sleeve, then centrifuge and test the pellet.
