CHAPTER 37. Infectious Diseases
Rebecca S. McConnico
BLOOD-BORNE AGENTS
I. Equine infectious anemia (EIA)
A. EIA is caused by a virus classified in the lentivirus genus of the Retroviridae family
B. Once infected with this virus, a horse remains infected for life
C. Acute infection is associated with fever and lethargy
D. Some horses will exhibit anemia and thrombocytopenia
E. Most horses recover from this initial febrile episode but may undergo recurring febrile episodes associated with periodic emergence of novel antigenic variants of the virus
F. In some horses these episodes become more severe and the horse develops classic clinical signs of EIA:
1. Weight loss
2. Ventral edema
3. Fever
4. Lethargy
5. Anemia
6. Thrombocytopenia
7. Hyperglobulinemia
G. In most horses, however, the febrile episodes become less frequent and less severe and the horse becomes an inapparent carrier of the virus. Inapparent carriers are normal on physical examination but often have subtle clinicopathological alterations suggestive of ongoing viral activity:
1. Increased serum globulin concentrations
2. Decreased albumin:globulin ratio
3. Intermittent thrombocytopenia or mild anemia
H. EIA transmission
1. EIA virus is most commonly transmitted by the intermittent feeding of hematophagous insects, especially biting flies of the genus Tabanus (horseflies) or Chrysops (deerflies)
2. Flies are strictly mechanical vectors, and virus does not live long outside the horse
3. Mosquitoes are unlikely to transmit EIA virus for the following reasons:
a. Mosquitoes do not elicit a painful bite to a horse; thus, feeding pattern is not interrupted
b. Mosquito saliva adversely affects EIA virus viability
c. The mosquito’s mouth parts are not large enough to contain an infective dose of EIA virus
d. For transmission to occur, a fly must begin a blood meal on an infected horse, be interrupted, and immediately resume feeding on an uninfected horse
e. EIA virus may also be transmitted transplacentally, especially if a pregnant mare experiences febrile episodes during gestation
f. Transmission via ingestion of colostrum or milk from an infected mare is possible but not likely
g. Venereal transmission is rare
h. Iatrogenic transmission may occur through the use of shared needles for injections or use of improperly sterilized surgical instruments or other devices that contact equine blood
I. Prevention of EIA
1. All horses on a farm should be tested at least yearly for the presence of antibodies to EIA virus
2. Presence of antibodies indicates that a horse is infected and will remain infected for life
3. EIA virus–positive horses should be permanently quarantined or euthanized. All new arrivals to a farm should be recently EIA virus–negative before arrival on the farm
4. Farm management practices should attempt to minimize fly populations through appropriate trash and manure disposal and judicious use of chemical or nonchemical insect control programs
5. Horsefly bites are usually most numerous during daylight hours in wooded areas. Pasture turnout schedules should take these facts into consideration
6. Horse owners and veterinarians should strictly adhere to the “one needle, one horse” rule. All instruments that come into contact with equine blood should be thoroughly disinfected before use on another horse
7. Horse owners and veterinarians should encourage organizers of equestrian events to require proof of a negative EIA test for all horses before participation in those events
A. Caused by one of two species of hemoprotozoal parasites: Babesia caballi or Babesia equi
B. Intraerythrocytic parasites transmitted primarily by tick vectors
C. Within 1 to 4 weeks of exposure previously unexposed horses develop signs of
1. Fever
2. Depression
3. Dyspnea
4. Pale or icteric mucous membranes
5. Ecchymoses of the nictitating membrane
6. Constipation
7. Colic
8. Dependent edema
D. Massive infection results in classic signs of intravascular hemolysis:
1. Icterus
2. Hemoglobinemia
3. Anemia
4. Hemoglobinuria
5. Hyperbilirubinemia
E. Clinical signs in horses infected with B. caballi last a few days to a few weeks and mortality is low
F. Most horses spontaneously clear the organism after 12 to 42 months of infection
G. Infection with B. equi is more severe, and horses may die within 24 to 48 hours of the onset of clinical signs
H. Infection is usually lifelong unless the horse is treated
I. In endemic areas, it is desirable to suppress clinical signs of disease without eliminating the organism from the horse
J. As with some other protozoal infections, effective immunity depends on continual exposure to the organism (premunity)
K. Imidocarb dipropionate or buparvaquone is effective for treatment of clinical signs of babesiosis in horses
L. Babesia caballi infections are easier to eliminate than are B. equi infections
III. Equine granulocytic ehrlichiosis
A. Caused by Ehrlichia equi, a rickettsial organism that resides in equine neutrophils and eosinophils
B. Clinical signs
1. Fever
2. Anorexia
3. Depression
4. Petechia and ecchymoses
5. Icterus
6. Ventral edema
7. Ataxia that lasts 3 to 16 days
C. Infected horses are usually:
1. Thrombocytopenic
2. Leukopenic and anemic
3. Clinical signs are most severe in adult horses and foals may experience only a mild fever
D. Diagnosis and treatment
1. During acute stages of the infection, granular inclusion bodies may be seen in the cytoplasm of neutrophils and eosinophils on blood smears routinely stained with a Wright’s-Giemsa type stain
2. These inclusions are pleomorphic, blue-gray to dark blue spoke-wheel shapes representing a cluster of coccobacillary organisms within cytoplasmic membrane-bound vesicles
3. A fluorescent antibody test is available for detection of antibody to the organism
4. A fourfold change in acute and convalescent titers is considered diagnostic of infection
5. Mortality is rare, and most untreated horses recover over a period of 2 weeks
6. Recovery may be hastened by treatment with intravenous (IV) oxytetracycline at 7 mg/kg once or twice daily for up to 7 days
NEUROLOGIC DISORDERS
I. Equine protozoal myelitis (EPM)
A. Definition: A debilitating neurologic disease of horses that can affect the brain, brainstem, spinal cord, or any combination of these three areas of the central nervous system (CNS)
B. Clinical signs may suggest focal or multifocal disease, which means that the disease may affect a very small (focal) part of the CNS or many parts of the CNS (multifocal)
C. The disease may present itself with a variety of different clinical signs, dependent on the location of the damage caused by the organism within the CNS. No vaccine is currently available
D. Life cycle
1. Causative organism: Although EPM has been recognized since the 1970s, it was not until 1991 that the organism (protozoan parasite) was cultured from a horse and given the name Sarcocystis neurona
2. The horse is a dead-end aberrant host, as infectious forms of the parasite are not passed from horse to horse or from horse to the definitive or true intermediate hosts
3. Recent investigation indicates that opossum feces (definitive host) are the source of the infection for horses, although other sources include several other mammalian species, including cats, skunk, raccoon, and others
4. Opossums acquire the infection by eating infected birds (intermediate hosts)
5. Most infections come from contaminated pasture, hay, grain, and water with opossum feces. Contamination of feed and water with opossum feces may occur indirectly through other mechanisms such as birds and insects
6. Control of the parasite to prevent infection of horses will be a daunting task because of the wide distribution of definitive and intermediate hosts in the environment of horses. Relocation of opossums away from horses, water, bedding, and feed storage environments may be beneficial to reduce exposure
E. Occurrence
1. EPM occurs in much of North America
2. Surveys conducted have revealed that approximately 50% to 80% of horses have been exposed to this parasite
3. A positive serum test indicates exposure to the parasite, not necessarily the presence of disease
4. In the studies that looked at the distribution of seropositive cases geographically, it was found that climatic factors may affect exposure rates; that is, an increase of freezing days was associated with a decrease in numbers of horses exposed to the parasite. A similar effect of very hot environments may also decrease the survival of the infective stages of the protozoan parasites and lessen exposure to horses. EPM appears to have a sporadic distribution, although outbreaks have been reported
F. Clinical signs
1. A progressive disease which if not treated may eventually lead to death
2. Any horse that is demonstrating neurologic abnormalities may have EPM
3. The clinical signs depend on the location of the organism within the CNS. EPM can affect a horse of any age, breed, or sex
4. Clinical signs may be triggered or worsened by physiologic stress or the administration of corticosteroids
5. Clinical signs of the disease:
a. Weakness
b. Malposition of a limb
c. Muscle atrophy
d. Spinal ataxia or “wobbling”
e. Head tilt with asymmetry of the face (eyelid, ear, lip)
f. Severely affected horses may be down and unable to rise
g. Lameness not traceable to orthopedic disease or any combination of the above signs may occur in early or less severe infections
h. Other unusual signs may occur
6. Typical case
a. Affected horses are bright and alert with a normal appetite
b. Some horses are dysphagic (unable to eat) and may act as if they are choked, with feed material coming from their nose
c. Hematologic and biochemical blood values are usually in the normal range
d. Sometimes a horse may have more than one disease, for example, both EPM and cervical stenotic myelopathy (“wobbler”)
G. Diagnosis
1. Based on clinical signs and on testing of the horse’s cerebrospinal fluid (CSF)
2. A positive serum test cannot be used to make a diagnosis but simply indicates exposure to the parasite, not necessarily the presence of the disease
3. CSF testing is now believed to be the most useful test to assist in the diagnosis of this disease in the live horse
4. The western blot test of CSF detects antibodies that the horse has formed against the parasite. The presence of these antibodies in the CSF of horses with neurologic signs usually indicates active disease. However, if blood contaminates the CSF sample, a false-positive test is a likely result. Positive CSF tests among horses without neurologic signs have occurred; however, the significance of these findings has not been determined. If the test is negative, and the horse is exhibiting clinical signs, the horse may still have the disease. Acupuncture is not recognized as an accurate diagnostic test
H. Therapy
1. Treatment of horses with EPM is expensive
2. The average range of treatment is 90 to 120 days and may exceed 6 months in some instances
3. The appropriate length of treatment and the method to determine adequate treatment duration are unknown
4. The current approved approaches to treatment:
a. Ponazuril (Marquis, Bayer Pharmaceutical) 5 mg/kg every 24 hours × 28 days
b. Nitazoxinide (Navigator, Idexx Pharmaceuticals), 25 mg/kg days 1 through 5, then 50 mg/kg days 6 through 28
5. Frequent, periodic, veterinary neurologic examinations during the treatment period. Discontinuation of therapy may be based on administration of medications 30 days beyond the plateau of clinical improvement. An alternative approach to determining discontinuing of therapy is disappearance of antibody to the protozoa from the CSF. Suboptimal dosing of intermittent therapy has no proven efficacy
6. Adverse side effects of therapy may include the following:
a. Anemia
b. Abortion
c. Diarrhea
d. Low white blood cell count
7. Medications for treatment of EPM inhibit folic acid metabolism. Supplementation with folic acid (40 mg per os [PO], once a day) may help prevent adverse side effects. Folic acid should not be administered at the same time as the antimicrobial drugs
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