LEPTOSPIROSIS
Aetiology
Leptospirosis in cattle may be caused by non– host-specific serotypes such as Leptospira Pomona, Leptospira icterohaemorrhagiae, and Leptospira canicola or host-specific c types such as Leptospira hardjo. Pathogenic leptospira are now divided into 13 named species and four genomospecies based on DNA-DNA reassociation studies, with Leptospira interrogans being the most common. The species are further divided into serovars/ serogroups and then into strains. The two genospecies L. interrogans and Leptospira borgpetersenii are most important in cattle. Six serovars have been identified in cattle in the United States: Pomona, canicola, icterohaemorrhagiae, hardjo, grippotyphosa, and szwajizak. L. borgpetersenii hardjobovis appears to be the most common serovar of cattle in the United States. Leptospira australis and Leptospira hebdomads also have been identified in cattle in Japan.
Leptospira spp. is spirochetes that are considered saprophytic aquatic organisms, and those pathogenic for humans and animals do not appear to multiply outside the host. Infection occurs by penetration of the organism through the mucous membranes of the conjunctiva, digestive tract, reproductive tract, skin wounds, or moisturedamageduterus, and establishment of renal infection. Most Leptospira spp. colonize the renal tubules and are shed in urine for variable periods following infection. Many natural domestic and wild reservoirs of L. interrogans exist that can shed the organism into the environment of cattle. It is difficult to blame any single species in all instances because most of the serotypes are not host-adapted. Dogs, swine, rats, mice, horses, deer, and other wild animals may contaminate the environment of susceptible cattle. Cattle are the maintenance host of L. hardjo and appear to be the only reservoir. Following infection and bacteremia, immunoglobulin (Ig) M antibodies that are agglutinins appear within a few days, whereas IgG antibodies with neutralizing activity appear later.
Although agglutinating
antibodies help clear the bacteremia, they do not result in the resolution of residual
renal infection. Non–host-adapted Leptospira spp. may persist in cattle
for 10 days to 4 months. The clinical consequences of leptospira infection in cattle
include both septicemic and reproductive disorders, but many leptospiral
infections are subclinical and detected by serologic evidence or by the presence of
lesions of interstitial nephritis at slaughter. The exact prevalence of leptospirosis
is not known, but serovar infection seems to be increasing,
whereas serovar Pomona infection rates seem to be decreasing. Some
estimates suggest herd infection prevalence in U.S. dairies is between 35% and
50%, mostly attributable to serovar hardjo.
Clinical Signs
Both
experimental and natural infections with L. Pomona have an incubation
period of 3 to 9 days. Acute leptospirosis with L. Pomona is most
common in calves but can
be
seen in adult dairy cattle. Calves have an acute onset of fever (104.0 to
107.0° F/41.11 to 41.67° C), septicemia, hemolytic anaemia, hemoglobinuria,
inappetence, increased heart and respiratory rates, and depression. Petechial
haemorrhages and jaundice also are possible. Mortality is high in calves less
than 2 months of age. Adult cattle with acute L. Pomona infections are
septicemic, have a high fever and a complete cessation of milk flow, accompanied
by a slack udder with a characteristic thick mastitis secretion that is red,
orange, or dark yellow in all quarters. Adult cattle may show haemoglobinuria and
may abort during the septicemic phase. Subacute or chronic infections are most
common in adult dairy cattle and, unless fever, hemoglobinuria, jaundice, or mastitis appears,
may go undiagnosed unless epidemic abortions occur. Abortion usually happens
several weeks—on average 3 weeks following septicemic infection of the fetus,
and a cluster of animals may abort within a few days or a few weeks. Aborted
fetuses characteristically are in the last trimester of pregnancy but can be
anywhere from 4 months gestation to term. Calves infected in utero during the
terminal stages of gestation may be born weak or dead. Because abortion follows
infection for such a long time, aborted fetuses are dead and maybe somewhat
autolyzed. It follows that serum collected from the aborting cow usually will
show seroconversion and, in effect, be a convalescent titer because the cow was
infected several weeks earlier. Certain geographic areas that support L.
interrogans serovar Pomona or other serovars pathogenic to cattle
have a high incidence of leptospira abortion unless intensive vaccination is
practised. Heifers allowed access to pasture typically aborts in late summer or
early fall in the northeastern United States. Failure to establish adequate
primary immunity in bred heifers that are pastured is the leading management problem
predisposing to abortion in this area. A different situation occurs in free
stalls, where infection can occur at any time of the year in susceptible cattle
exposed to the organism. Recently L. borgpetersenii serovar hardjo has
been reported to cause an epidemic or endemic reproductive problems
in
cattle in the United States. Definitive proof of a causative relationship
between L. hardjo infection and abortion in cattle is lacking! This
host-associated serovar (hardjo) may have pathogenesis slightly
different from other serovars in cattle in that L. hardjo primarily
infects the uterus and mammary gland following septicemia. The subacute to the chronic form of infection is most commonly associated with reproductive
problems. Studies have demonstrated that cattle naturally infected with L.
borgpetersenii serovar hardjo can shed the organism in their urine
for indefinite periods, with the maximal shed occurring early in infection. Acute systemic signs are possible when the
disease is introduced into a herd and include fever, depression, inappetence,
and a flaccid udder that secretes thick yellow to orange milk from all
quarters. Abortion is believed to occur most commonly 4 to 12 weeks following the initial infection of pregnant cows. Subclinical infection and possibly abortion
are most likely in herds having an endemic infection caused by L.
borgpetersenii serovar hardjo. Such endemic herds may have resistant
adult cows but persistent reproductive problems in first-calf heifers joining
the herd. Infertility and early embryonic death are seen with increased
services per conception, prolonged calving intervals, and delayed return to
heat. The organism is shed from the reproductive tract for several days
following abortion and persists in the oviducts and uterus of infected cows for
prolonged periods of weeks to months. In addition, the organism can be cultured
from the oviducts up to 3 weeks following abortion or calving. Venereal spread also
is possible in bull-bred herds.
Diagnosis
For
acute infections in young calves showing hemoglobinuria, water intoxication is the
major differential. Adult cattle showing acute septicemic disease and skin.
Hematogenous spread of the organism can result in seeding of multiple organs, including hemoglobinuria require differentiation from many diseases, including postparturient
hemoglobinuria, bacillary hemoglobinuria, babesiosis, hemorrhagic cystitis associated
with malignant catarrhal fever (MCF), enzootic hematuria, pyelonephritis, and
other diseases causing “red urine.” Seroconversion assessed by comparative acute
and convalescent titers is the best diagnostic proof of infection. Although
several antibody tests are available, the microscopic agglutination test and enzyme-linked
immunosorbent assay (ELISA) are used most commonly. FA techniques or darkfield examination also can be used to detect leptospira in urine during acute infections
with L. interrogans serovar Pomona. A fourfold increase in
convalescent titer over acute titer is considered significant and is even
expected with most serovars. Vaccination of cattle generally causes a
relatively low agglutination titer (400 or usually less). Leptospira
borgpetersenii serovar hardjo does not play by the same rules,
however, and titers are more difficult to interpret and quite variable. Titers
of antibodies against serovar hardjo may be low or negative at the time of the abortion. Because aborted fetuses are long dead and autolyzed,
they generally are not helpful to the diagnosis. Therefore serology is indicated for abortion epidemics suspected to be L. interrogans serovar Pomona or other nonhardjo serovars and serology coupled with detection of the organism in uterine tissue, fluids, or urine in L. borgpetersenii serovar hardjo abortions. Leptospires or their DNA can be detected by culture, immunofluorescence, special stains of tissue, or polymerase chain reaction (PCR) assay.
Treatment
Acute
cases caused by L. interrogans serovar Pomona can be treated with
tetracycline or tilmicosin. Because streptomycin has been withdrawn from the
market and causes prolonged meat residues, this highly successful treatment in
cattle no longer can be recommended. Whole blood transfusions and IV fluids
may be necessary supportive measures in the treatment of acute septicemic calves
or cattle. L. hardjo has been treated successfully with a single dose of
long-acting oxytetracycline at 20 mg/kg IM, tilmicosin at 10 mg/kg SQ, or
multiple injections of ceftiofur sodium (2.2 or 5 mg/kg IM, once daily for 5
days, or 20 mg/kg IM, once daily for 3 days). All have some efficacy in
eliminating urinary shedding of L. borgpetersenii hard. Amoxicillin
administered IM at 15 mg/kg, in two doses 48 hours apart, has likewise been
shown to eliminate shedding of L. borgpetersenii hardjo in urine.
Following treatment of shedding heifers with a single dose of amoxicillin at 15
mg/kg, no leptospires were isolated from the kidneys at slaughter.
Prevention
Because
treatment of leptospirosis often is unsuccessful, prevention using vaccination
is imperative. Whole-cell bacterins must be serovar specific for protection to
occur. Five-way leptospirosis bacterins (Pomona, canicola, icterohaemorrhagiae,
grippotyphosa, and hardjo) are most commonly used. Effective
prevention against these serovars— except hard—is
possible when primary vaccination of calves is followed by twice-yearly
boosters. Calves should be vaccinated after maternal antibodies have diminished
at 4 to 6 months of age, and two doses of vaccine are essential to establish
primary immunity. Boosters are administered at 4- to 6-month intervals thereafter.
The most common mistake that prevents effective vaccination is administering a
single dose of bacterin to heifers and then not giving them booster shots until
6 to 12 months later, thereby never affecting primary immunization. Effective
immunization against L. borgpetersenii serovar hardjo is more
difficult, and only a few vaccines have demonstrated efficacy against L.
hardjo infections. Monovalent serovar hardjo vaccines have
been shown to protect cattle from infection, whereas pentavalent vaccines have
not. Currently available monovalent vaccines formulated with L.
borgpetersenii serovar hardjo (Spirovac,. Pfizer Animal Health, New
York, NY, and Leptavoid, Schering Plough, Coopers Animal Health, Wellington,
New Zealand) have been demonstrated to induce both humoral IgG responses and
cellular immune responses that confer protection against L. hardjo infection.
Although proven disease due to L. hardjo is controversial, vaccination
is recommended because other control measures are not available. Isolation of
aborting or acutely ill cattle and prompt removal of aborted fetuses may
decrease the spread of the organism but is seldom a practical means of control. Antibiotic
treatment to eliminate the organism in infected cattle should be part of the
control strategy because vaccination will not eliminate the infection.
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