edema and vascular damage throughout the body.

There is hemorrhagic

Chapter 1
Infectious diseases
necrosis and gross swelling of all the lymphoid organs.

Diagnosis
In many countries anthrax is a notifiable disease, and even a suspicion of
its possible occurrence must be reported to the appropriate authorities.
Diagnosis in a freshly dead animal is made in the first instance by micro-
scopic examination of blood smears.
The blood should be collected from a small superficial vein (such as the
cephalic) that is likely to ooze little when opened. Swabs of this blood are also
normally required. Any leakage from the vessel should be staunched with
swabs soaked in strong disinfectant or the vessel should be cauterized. The
smears should be reasonably thick and lightly fixed before staining with poly-
chromatic methylene blue (or Giemsa). The slides should be handled with cau-
tion because spores are likely to be present. The presence of blue, square-ended
bacilli surrounded by large pink capsules, which frequently have frilly edges,
is conclusive. These bacilli are often in short chains. B. anthracis can readily be
isolated from the swabs either directly or by scarifying the skin of a laboratory
animal such as the guinea pig with the swab.

Treatment and control

B. anthracis is very sensitive to a wide range of antibiotics, including penicillin
and the tetracyclines. Penicillin is curative if administered in massive doses
(40 000–80 000 IU/kg IV q.i.d.) to an animal in the early stages of the disease,
before the toxin has produced irreversible damage. They also prevent the
development of the disease in other animals within a group deemed to be at
risk from exposure to a common source of infection.
In areas where the disease is known to constitute a more or less continuous
threat, annual vaccination of all grazers is necessary. The Sterne vaccine con-
tains viable spores, which produce living cells of B. anthracis that lack the genes
that encode the capsular material. They cannot therefore encapsulate when they
germinate in vivo. Such cells survive only briefly when the spores are inoculated
into animals but they live long enough to elaborate toxin. Both Factors II and III
are immunogenic and stimulate antibody production. Antibody to the receptor-
binding molecule (Factor II) prevents Factors I and III from acting on cells.
If there is even the slightest reason on clinical grounds to suspect anthrax,
great circumspection is required in handling the case to minimize the risk to all
the people and any other animals directly or indirectly associated with it. The
carcass should not be the subject of a post mortem examination for this proced-
ure favors a massive release of spores into the environment. Control measures
vary in detail from country to country but always include prompt and effective
disposal of infectious carcasses, disinfection of buildings, bedding and equip-
ment, and quarantining of contacts, with additional controls on their produce.

STREPTOCOCCAL INFECTIONS
Etiology
Streptococci are probably the most frequently isolated bacterial pathogens of
Equidae. The species and subspecies usually encountered are S. equi subspecies

75
 equi, S. equi subspecies zooepidemicus and S. dysgalactiae subspecies equisimilis.
Bacterial diseases of the older foal and adult

These organisms belong to Lancefield group C, are beta-hemolytic and are

readily distinguished by their fermentation behavior in lactose, sorbitol and
trehalose as well as by the reactivities of their M-like proteins with specific
antisera.
S. equi is the most host adapted and causes strangles (q.v.), a suppurative
lymphadenitis of the head and neck of horses of all ages. It is also the most
highly conserved with almost no variations in M (SeM) and other proteins. In
contrast, strains of S. zooepidemicus have highly variable M-like (SzP) proteins
and other characteristics, are not host adapted, and are identified from a var-
iety of opportunist infections. S. equisimilis is the least commonly isolated
equine group C streptococcus and is occasionally isolated from uterine or pla-
cental samples and from abscessed lymph nodes and arthritic joints. Equine
strains show antigenic variation.
Alpha-hemolytic streptococci have been isolated from aborted fetuses and
from lesions of funisitis and placentitis. S. pneumoniae capsule type III has
been isolated from the airways of young horses in training.

Epidemiology
The highly host-adapted S. equi is maintained only in horse populations in
which clinical disease is occurring. However, it survives in water for about 30
days and for extended periods in moist discharges. Nevertheless, persisting
contamination of the environment is not an important source of the organism
in outbreaks or in interepizootic maintenance. Prolonged carrier states asso-
ciated with guttural pouch empyema (q.v.) are found in some herds, although
the organism commonly disappears from horses in geographic regions for
long periods of time only to reappear when an infected horse is introduced.
Horses of all ages are affected but the disease is most common and most
severe in young horses. Pre-existing immunity may ameliorate expression of
the disease. S. equi is transmitted when discharges from the nose or abscesses
contaminate feed or water or when affected foals suckle the mammary gland.
Direct nose to nose contact may also result in transmission and contributes to
the highly contagious character of strangles.
In large groups of horses on breeding farms the most severely affected age
groups are foals, weanlings and yearlings. Morbidity in this age group may be
up to 100% with a mortality of 1–5%. Older animals show a lower morbidity
and mortality.
S. zooepidemicus occurs widely as a mucosal commensal of the nasopharynx
and external genitalia of the horse and other host animals. An opportunist
pathogen, it invades mucosal and epithelial surfaces damaged by virus infec-
tion or injury. It is the most commonly encountered pyogen in the horse and is
isolated frequently from infected wounds and injection sites of older horses
and from the umbilicus of foals in the first days of life. S. zooepidemicus is pre-
sent in approximately 50% of cases of cervicitis and endometritis (q.v.) in the
mare, in which it rapidly replaces E. coli that enters the reproductive tract devi-
talized by dystocia. Pneumovagina, retained placenta (q.v.) or an endocrine
abnormality such as anestrus associated with pseudopregnancy (q.v.) are other
abnormalities that predispose to invasion by S. zooepidemicus.

76
 Although showing ⬎97% DNA homology with the highly uniform (clonal)

Chapter 1
Infectious diseases
S. equi, S. zooepidemicus shows great variation in its SzP protein and in its
colony morphology. In epizootics of nasal catarrh in young horses, isolates
of the organism usually produce mucoid colonies with similar SzP proteins,
suggesting that more virulent clones have been selected and become
widespread.

Pathogenesis and clinical findings

S. equi enters the horse via the nose and mouth and attaches to cells in the
crypt of the lingual and palatine tonsils. In a few hours it penetrates and is car-
ried to one or more of the lymph nodes that drain the pharyngeal/tonsillar
region. Multiplication occurs extracellularly in the lymph node resulting in
the formation of long chains of the organism. Large numbers of neutrophils
are drawn to the site by complement-derived chemotactic factors. Failure of
phagocytosis and killing of the streptococcus appears to be due to a combin-
ation of the hyaluronic capsule, antiphagocytic SeM, and Se18.9 proteins.
The incubation period varies from 3 to 14 days after exposure, and clinical
signs include sudden onset of fever (39.5–40°C) caused by the pyrogenic exo-
toxin SePE-I, loss of appetite, halitosis, difficulty in swallowing, intermittent
cough, extension of the head and neck, swelling in the submandibular and/or
supralaryngeal areas, nasal discharge and inflammation of the lymphoid
nodules of the soft palate and tonsillar areas. During the following 3–7 days
the swelling in the intermandibular or suprapharyngeal areas may increase
because of lymphostasis and enlargement of the affected lymph node(s).
The occlusive effect of the lymph node enlargement is the source of the
disease description “strangles”, which in severe cases may result in suffoca-
tion unless emergency tracheotomy is performed. In most cases abscesses in
affected lymph nodes rupture 7–14 days after the first clinical signs.
Suprapharyngeal lymph node abscesses usually drain into the pharyngeal
area resulting in a copious nasal flow of purulent material. This drainage
may also occur into the guttural pouch, which may become distended and
palpable posterior to the vertical ramus of the mandible.
Metastasis of purulent material may result in abscess formation in other
locations such as the lungs, brain and thoracic or abdominal lymph nodes. This
complication has a poor prognosis and is commonly termed “bastard stran-
gles” (q.v.). Other complications during and after recovery from the typical dis-
ease include purpura hemorrhagica (q.v.), an immune complex-mediated
vasculitis that occurs at 1–4 wk, paralysis of the left recurrent laryngeal nerve,
anemia possibly associated with hepatic clearance of immune complexes
bound to erythrocytes, and myopathy characterized by coagulative necrosis or
chronic rhabdomyolysis and atrophy.
Outbreaks of strangles in horse populations with pre-existing antibody to
S. equi may be present as an atypical or catarrhal form of the disease charac-
terized by a slight purulent nasal discharge, cough, occasional slight fever of
short duration and abscessation of lymph nodes in a few affected animals. Its
progression in a group of horses is much slower than that of the typical dis-
ease. Older horses experiencing a secondary infection often exhibit the
catarrhal form of strangles.

77
 Approximately 70% of animals develop a solid, enduring immunity to the
Bacterial diseases of the older foal and adult

typical disease following recovery from strangles. This immunity is asso-

ciated in part with mucosal IgG and IgA, and serum opsonic antibodies.
Opsonic antibodies are slow to develop and do not attain adequate titers until
6–8 wk after clinical signs appear. Immunity is expressed in the tonsil and
blocks further invasion. Nasal shedding of S. equi may continue for 3–4 wk
following appearance of clinical signs and the organism may remain in the
guttural pouch of some recovered animals for months thereafter.
S. zooepidemicus is a constant secondary invader of the upper respiratory
mucosa as a sequel to influenza or herpes viruses. Many small purulent foci
are produced in the lymphoid follicles of the mucosa and the resulting nasal
discharge is mucopurulent. The draining lymph nodes often become enlarged
and hardened and may become abscessed in some animals, but abscessation is
much less frequent than in the case of strangles. Affected animals have nasal
and ocular discharges, cough, may be slightly febrile and lose body condition.
Secondary pneumonia due to S. zooepidemicus occurs in a portion of foal popu-
lations infected with influenza virus and is responsible for much of the
morbidity and mortality in this age group. In donkeys, these secondary pneu-
monias are often fatal.
S. zooepidemicus is occasionally isolated from lesions of pleurisy or peritonitis.
It is a common cause of joint ill (q.v.) in foals that may acquire infection in the
birth canal. The organism enters the umbilicus and the ensuing bacteremia
results in synovial infection, pyoarthritis and permanent damage to the joint(s).
In the mare, S. zooepidemicus infections of the cervix and uterus are transient
and occur shortly after parturition. Dystocia or retention of the placenta (q.v.)
may result in more persistent infections. However, most mares will recover
from endometritis if they go through one or two estrous cycles free of new
entry of bacteria into the uterus.

Prevention
The very contagious nature of strangles makes control of spread very difficult.
Clinically affected animals as well as animals detected as infected by culture
of nasal swabs or washes should be isolated immediately. The first clinical
sign is sudden onset of fever to 39.5–41°C. Animals at this stage are not shed-
ding S. equi and so may be isolated before transmission to others has occurred.
Twice-daily temperature taking is therefore an invaluable aid in minimizing
transmission and containing an outbreak.
All containers used for feed or water should be cleaned and disinfected.
Surfaces of stalls contaminated with discharges should be similarly cleaned
and disinfected. Effective disinfectants are povidone iodine, chlorhexidine
gluconate, 0.6% sulfuric acid, glutaraldehyde and phenol (1:200).
Where possible, fly infestations should be reduced by use of screens, insecti-
cides and electronic bug poppers. Contaminated bedding should be removed
to a protected location and covered with a plastic sheet to compost. Cases held
in isolation should be handled last and the animal attendant should be meticu-
lous about hand and arm washing, removal of coveralls and boots, etc., before
leaving the isolation area. Pasture upon which cases have grazed should be
rested for at least a month before being grazed again by horses.

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 In large breeding enterprises, weanlings and yearlings should be located in

Chapter 1
Infectious diseases
small geographically separated groups remote from areas where mares and
stallions are held. Incoming animals should be held in a designated isolation/
holding area for 2 wk before release into a group on the farm. Ideally, these ani-
mals should be subjected to one or more nasal swab cultures during the 2 wk
isolation period and rectal temperatures taken twice daily. This aspect of con-
trol cannot be overemphasized as the usual source of S. equi for uninfected
premises is the recently introduced infected animal. Nurse mares frequently
introduce infection in this way and should be isolated with their adopted foals.
Antibiotics such as a long-acting penicillin administered parenterally, e.g.
benzathine penicillin (30 000 IU per kg IM q 2 days), or feed supplementation
with low levels of tetracycline (60–80 ppm feed) are very effective in prevent-
ing or stopping an outbreak. However, herd immunity will not develop dur-
ing this time and animals will be highly susceptible to infection when the
antimicrobial drug is withdrawn. Use of low-level tetracycline also carries a
slight risk of antibiotic-induced clostridial enterocolitis (q.v.) should the horse’s
environment be contaminated with toxigenic strains. Penicillin administration
is most effective at the onset of fever before abscess development.
Vaccination with acid-extracted M protein or mutanolysin-extracted M pro-
tein commercial vaccines is effective in stimulating serum opsonic antibodies
when administered in a course of two inoculations. However, these vaccines
do not confer a high level of protection in the field against natural challenge. At
best, the number of clinical cases is reduced by half and the disease is less
severe in those cases that develop. Bacterin-type vaccines often elicit local and
systemic reactions to peptidoglycan in bacterial cell walls; M protein extract
vaccines contain less peptidoglycan and are better tolerated.
The incomplete protection stimulated by commercial vaccines is probably
related to failure to stimulate mucosal IgG and IgA antibodies. Vaccination
with live avirulent organisms is often effective in stimulating these antibodies
and a high level of resistance to experimental challenge results. However,
given that recovery from the naturally occurring disease provides solid pro-
tection in only 70% of horses, it is unlikely that vaccines based on live aviru-
lent organisms will protect a much higher percentage than this. Live vaccines
have the disadvantage that they may cause large painful abscesses if acciden-
tally introduced into muscle at remote injection sites.
Vaccination of mares has been shown to increase colostral titers of IgG anti-
bodies to SeM protein. Serum titers of these antibodies in suckling foals may
thereby be increased.
The multiplicity of M-like (SzP) protein types involved suggests that vac-
cines developed against S. zooepidemicus or S. equisimilis must be multivalent
or based on conserved epitopes or antigens.

Diagnosis
The clinical signs of classical strangles in which lymphadenitis is exhibited are
easy to recognize. A pronounced leukocytosis with neutrophilia and fibrino-
genemia accompanies the fever. However, bacteriologic examination is essen-
tial to confirm the diagnosis. Moist nasal swabs may be used to sample the
medial nasal mucosa 10–15 cm in from the external meatus of each nostril and

79
 plated on colistin–nalidixic acid (CNA blood agar). Nasal washes obtained by
Bacterial diseases of the older foal and adult

instilling warm physiologic saline (50 mL) into the retronares and collecting the
washings that drain into a disposable cup for culture are more sensitive than
swabs in detection of S. equi since a much larger area of the mucosa is sampled.
The polymerase chain reaction (PCR) using primers from the sequence of
SeM is now widely used in presumptive detection of S. equi in clinical samples.
The PCR test is approximately three times more sensitive than culture and is
highly specific. However, in chronic cases of guttural pouch empyema, S. equi
DNA may persist for days or weeks following bacteriologic cure.
Pus may also be aspirated aseptically from lymph nodes with a needle and
syringe. Swabs or pus should be plated without delay. Beta-hemolytic colonies
are identified after incubation overnight at 37°C by a combination of Lancefield
grouping reaction and fermentation reactions in lactose, sorbitol and trehalose.
Assay of convalescent antibody to S. equi by ELISA is available in specialized
laboratories and is performed with recombinant SeM as antigen.
Serologic examination is helpful in detecting horses with internal abscesses
and in confirming a diagnosis of S. equi-associated purpura hemorrhagica
(q.v.). In both of these instances, very high levels of serum antibody are present.
Placentitis and metritis caused by either S. zooepidemicus or S. equisimilis may
be diagnosed in the laboratory by culturing swabs or specimens on CNA agar.
Uterine swabs, tampons or biopsies should be cultured, preferably between 10
and 14 days after ovulation. Tracheal aspirates cultured on CNA and stained by
the Giemsa method are important in the laboratory confirmation of respiratory
S. zooepidemicus infections of young horses.

Treatment
The equine group C streptococci are very sensitive to penicillin, ampicillin,
erythromycin, chloramphenicol, cephalosporins and tetracyclines. Gentamicin
resistance has been noted in S. zooepidemicus isolates from equine sources.
Where appropriate, strangles is usually treated with IM doses of penicillin of
up to 10 million units. Cases treated immediately at time of onset of fever will
respond within hours and usually do not develop abscesses. However, since
most cases recover uneventfully and develop enduring immunity, antibiotic
administration is usually reserved for relief of life-threatening lesions that are
intruding on the airway or for S. zooepidemicus infections in foals complicated
by pneumonia.
Although penicillin is very effective for prophylaxis of in-contact animals
and in treatment of respiratory tract disease caused by the equine group C
streptococci, use of antibiotics requires careful consideration as they may
delay maturation and draining of abscesses and ablate the protective immune
response.
Abscesses should not be opened surgically until the capsule and fluid con-
tents can be readily palpated beneath the skin. Insertion of a 16 or 18 gauge
needle through surgically prepared skin into the abscess often establishes
a tract along which the abscess capsule dissolves and speeds evacuation with-
out the need for surgical incision.
Supportive therapy of strangles cases includes twice-daily cleansing of
draining sites and nostrils, application of fly repellents and provision of a

80
high quality soft, moist feed. Guttural pouch infections (q.v.) may require

Chapter 1
Infectious diseases
irrigation with surgical antiseptic or penicillin solutions.
Streptococcal endometritis or placentitis may be treated with IM injections
of penicillin (22 000 IU/kg BW/day) for 2 wk. Streptococcal placentitis must
be treated at the first sign of vaginal discharge but with the caveat that the
fetus already may have become septicemic by the time the discharge is noted.
Treatment of chronic streptococcal endometritis (q.v.) is most effective during
estrus when the non-specific natural antibacterial clearance mechanisms are
most efficient.
Treatment of horses with purpura hemorrhagica includes corticosteroids to
reduce polymorphonuclear leukocyte responses and antibiotics to protect
against secondary bacterial infection. Blood transfusions (q.v.) may be indi-
cated in cases with anemia or thrombocytopenia. Edematous legs should be
bandaged.

CORYNEBACTERIUM PSEUDOTUBERCULOSIS
Etiology
Corynebacterium pseudotuberculosis produces a syndrome of ulcerative lymphan-
gitis or abscess formation. Folliculitis and abortion have also been reported. The
bacterium is a Gram-positive, non-motile facultative anaerobe that survives
well in the environment and can infect other species, including man.

Epidemiology
The disease occurs worldwide in areas where horses are raised. However,
there is a marked variation in clinical signs in geographic locations throughout
the world. Pectoral, ventral midline, abdominal and inguinal abscesses are fre-
quent presentations in areas of the western USA, whereas ulcerative lymphan-
gitis is more typical elsewhere. The incidence of disease varies from year to
year, and outbreaks can occur. Common names for the abscess form of the
disease are “pigeon fever”, “pigeon breast”, “dry-land distemper” or “Colorado
distemper”.
Folliculitis (contagious pustular dermatitis, “contagious acne” or
“Canadian horsepox”) caused by C. pseudotuberculosis results in pustules that
are often distributed in areas where tack or harness make contact with the
skin. The disease may be transmitted by contaminated grooming utensils.
Trauma to the skin, existing folliculitis or seborrhea may predispose the horse
to infection. Ulcerative lymphangitis is a fairly uncommon disease that is
usually associated with poor sanitation. Open draining tracts can be a source
of environmental contamination.

Pathogenesis
The organism finds a portal of entry through abraded mucous membranes or
compromised skin surfaces such as may be caused by badly fitting tack.
Biting insects may also provide a portal of entry. This phenomenon may
explain the seasonal incidence of the disease, particularly for the abscess form.

81