Vol.18, No.
11 November 1996
Continuing Education Article
FOCAL POINT
★Leptospirosis is an important
cause of acute renal failure in
suburban and urban dogs and
has zoonotic potential.
KEY FACTS
■ Vaccination can only provide
protective immunity against the
serovars in the vaccine.
■ Antibiotic therapy and aggressive
supportive care are usually
required before the confirmatory
diagnostic test results are
received.
■ Acute renal failure due to
leptospirosis is reversible with
early diagnosis and treatment.
■ Prolonged shedding of viable
organisms in urine poses a
zoonotic hazard to owners and
animal-care personnel.
Canine Leptospirosis
Auburn University
James S. Wohl, DVM
L eptospirosis remains an important infectious disease of dogs even
though leptospiral vaccines have been available for over 30 years. It is a
worldwide zoonosis with a low fatality rate in humans.
Classic leptospirosis, which is associated with the serovars icterohaemorrha-
giae and canicola, has been associated with acute or subacute hepatic and renal
failure in dogs.1 Common commercial vaccines contain antigens from these
serovars. Use of these leptospiral vaccines has been responsible for the decrease
in the number of icterohaemorrhagiae and canicola infections. Because leptospi-
ral vaccines are serovar-specific, however, they do not induce immunity against
other pathogenic serovars, such as grippotyphosa and pomona. The first box lists
Leptospira interrogans serovars that have been found to be pathogenic in dogs.
Recently, canine leptospiral infections due to serovars other than icterohaem-
orrhagiae and canicola have become more apparent in the pet population.2–5
Serovars grippotyphosa and pomona are leading infectious causes of acute renal
failure in dogs. Serovars bratislava, ballum, australis, hardjo, and bataviae have
been implicated in canine hepatic and renal disease worldwide.
The worldwide distribution of leptospirosis reflects the organism’s ability to
infect most species of warm-blooded animals. The regional distribution of spe-
cific serovars and the prevalence of infection reflect the migratory patterns of
wild mammal carriers and environmental conditions.
LEPTOSPIRES
Leptospira is a genus of spirochetes. All pathogenic leptospires are members
of the species Leptospira interrogans, although different species classifications
have been proposed.6 More than 200 serovars belonging to 23 serogroups of L.
interrogans have been identified.7 Many leptospires are adapted to specific
mammalian hosts8–11 (Table I).
Leptospires cannot replicate outside of a host. Most serovars replicate in the
kidneys of infected hosts and are shed in urine. In warm, wet climates, the or-
ganisms can survive for months in neutral to slightly alkaline water or urine-
saturated soil.12 Prolonged shedding of leptospires from the host is responsible
for the persistence of leptospires in the environment.
Outbreaks of human and canine leptospirosis have followed periods of heavy
rainfall or flooding.13 These outbreaks are probably due to optimum environ-
mental conditions for survival of the organism and the migration of infected
wild mammals into more populated areas. The sources of infection for dogs in
the urban and suburban United States are believed to be related to the move-
Small Animal The Compendium November 1996

ment of carrier animals, such ganisms rapidly invade the

as raccoons, opossums, skunks, DAY 0 Exposure to leptospires from bloodstream and tissue
squirrels, mice, and rats.2,14 contaminated water or (Figure 1).
mammalian sources
Pathogenicity Pathophysiology
The pathogenicity of a Penetration of mucous The leptospiremic phase
leptospiral infection depends membranes can persist for several days
on whether the host belongs to a week after exposure
to a maintenance or inci- and may be associated with
Leptospiremia
dental host species for the fever, depression, and myal-
serovar. Infections in inci- gia. 22,26 A toxin associated
dental hosts are associated Vasculitis with the organism’s outer
with more severe clinical dis- membrane has been impli-
ease and a shorter shedding cated in the pathogenesis
Penetration of organ tissues
phase. Several serovars have of tissue damage, but the
reportedly caused clinical DAY 7 identity of the toxin re-
disease in dogs.2,3,15–21 Replication in renal tubules mains unclear.27
The canicola serovar can Inflammation of blood
cause renal failure and hep- vessels and renal tubules is
DAY 14 Leptospiruria
atitis in dogs even though attributed to replication of
dogs are its maintenance the organisms.22 Dehydra-
host. Vaccination diminishes Carrier state tion results from lack of
the pathogenicity of canicola oral water intake and in-
in dogs but does not pre- creased fluid losses through
vent infection or the carrier Clearance of Chronic carrier damaged renal tubules, in-
state.22 Even vaccinated dogs leptospires state creased vascular permeabili-
can pose a zoonotic threat.23,24 ty, vomiting, and diarrhea.
Common serovars identified Figure 1—Pathogenesis of canine leptospirosis. Hemorrhagic diathesis and
in human cases of lepto- gastrointestinal signs in cas-
spirosis include pomona, es of icterohaemorrhagiae
canicola, icterohaemorrhagiae, hebdomdis, hardjo, au- infection have been reported and are attributed to vas-
tumnalis, and grippotyphosa.7 culitis and hypoxia secondary to the contraction of in-
Most leptospiral infections travascular volume.
may be subclinical. Host
Leptospira immune status and virulence CLINICAL SYNDROMES
interrogans of the infecting serovar are Classic Leptospirosis
Serovars more important determi- Although infection with most serovars can cause lep-
That Are nants of clinical disease than tospiremia and vasculitis, organ involvement is more
Pathogenic in Dogs is the number of invading serovar-specific. Classic icterohaemorrhagiae infection is
organisms.25 characterized by acute hemorrhagic disease or subacute
severe hepatic failure and uremia. Dogs are icteric, de-
■ australis
Routes of Infection pressed, and febrile and exhibit signs of muscle pain.
■ autumnalis Leptospires infect a host by Elevations in liver enzymes, bilirubin, urea, and creati-
■ ballum penetrating mucous mem- nine are common in subacute cases. Leukocytosis and
■ bataviae branes or entering through thrombocytopenia are also present in classic leptospiro-
■ bratislava skin abrasions after the host sis. Dogs infected with canicola are more likely to
■ canicola is exposed to contaminated exhibit acute interstitial nephritis with less hepatic in-
water, urine, or the carcass of volvement. Leptospirosis due to icterohaemorrhagiae or
■ icterohaemorrhagiae
an infected animal.7,22 Infect- canicola is more likely in puppies and unvaccinated
■ grippotyphosa ed meat has been reported as dogs.28
■ hardjo a source of infection, and The occurrence of classic leptospirosis has decreased
■ pomona venereal and transplacental in the United States with the use of a bivalent vaccine
transmission can occur.22 Or- (containing antigens from serovars icterohaemorrhagiae

SUBCLINICAL INFECTION ■ TISSUE DAMAGE ■ DEHYDRATION

The Compendium November 1996 Small Animal

TABLE I phosa commonly have a his-

tory of anorexia, depression, Common Clinical
Leptospira interrogans Serovars
and their Maintenance Hosts and vomiting. Decreased ac- Features
tivity and polyuria/polydip- of Canine
Serovar Maintenance Host sia may also occur. Physical Leptospirosis
examination findings (see
canicola Dogs
Common Clinical Features) Physical Signs
icterohaemorrhagiae Rats may include fever, renomeg- ■ Fever
aly, and lumbar pain sec-
■ Anorexia
grippotyphosa Raccoons, voles, ondary to enlarged and in-
skunks, opossums flamed kidneys. Some dogs, ■ Myalgia
however, have no physical ab- ■ Dehydration
pomona Cattle, pigs normalities on presentation. ■ Polyuria/polydipsia
Marked thrombocyto- ■ Hypovolemic shock
bratislava Pigs penia (25,000 to 150,000 ■ Peripheral edema
platelets/µl) is often present,
hardjo Cattle ■ Vomiting
although hemorrhage and
coagulation test abnormali- ■ Diarrhea
ballum Mice
ties are uncommon. 2 Vas- ■ Bleeding
culitis is probably respon- ■ Icterus
sible for the low platelet ■ Abdominal or lumbar
and canicola). Acute renal failure due to serovars not counts. Otherwise, hemo- pain
present in the bivalent vaccine has become the more grams are usually unremark-
■ Renomegaly
important clinical syndrome in vaccinated and unvacci- able except for possible mild
nated dogs. to moderate mature neutro- Laboratory
The increased presence of Leptospira-carrying wild philia. Abnormalities
mammals in areas populated by dogs is also probably Serum chemistry assays
■ Leukocytosis
involved in the recent epidemiology of canine lepto- usually reveal azotemia. How-
spirosis. In 1992, Rentko and coworkers reported a se- ever, urea and creatinine ■ Thrombocytopenia
ries of mostly suburban dogs with acute renal failure concentrations may be nor- ■ Elevated urea and
due to serovars pomona and grippotyphosa.2 Twelve of mal in the early phase of the creatinine
the dogs had previously been vaccinated against canico- disease. 2 Hepatic enzymes ■ Elevated hepatic
la and icterohaemorrhagiae. Nine of these dogs were (alanine transaminase, alka- enzymes
vaccinated during the 6 months prior to infection. The line phosphatase, and aspar-
■ Elevated total bilirubin
dogs in this study did not develop significant acute or tate transaminase) may be
chronic hepatic disease. The absence of hepatic disease significantly elevated. Total ■ Hypoalbuminemia
distinguishes infection with these serovars from classic bilirubin concentrations are ■ Increased or
leptospirosis due to icterohaemorrhagiae or canicola. normal or mildly elevated. decreased serum
Other serovars have also been reported to cause clin- Abnormalities in serum sodium, chloride,
ical disease in dogs. In Italy, titers directed against sodium, chloride, and po- or potassium
serovar bratislava were a common finding in a group of tassium concentrations may
concentration
dogs with signs consisting of depression, icterus, fever, reflect disturbances in renal
and anorexia.5 Bratislava was cultured from a dog with and gastrointestinal function. ■ Isosthenuria
mild clinical signs in the midwestern United States.3 Serum albumin concentra- ■ Hematuria
Asymptomatic interstitial nephritis was found to be the tions may be low because of ■ Urine sediment,
result of serovar hardjo infection in a group of laborato- leakage from damaged en- granular tubule casts,
ry beagles.20 dothelium, gastrointestinal and white blood cells
loss, decreased dietary in-
■ Glucosuria
Acute Renal Failure take, and decreased hepatic
Figure 2 outlines the steps in the diagnosis and man- synthesis.
agement of acute renal failure due to leptospirosis. Serial blood tests are war-
Physical abnormalities and history vary with the phase ranted because biochemical test results may change over
of infection. Patients infected with pomona or grippoty- the course of infection. Progressive azotemia is a more

THROMBOCYTOPENIA ■ ELECTROLYTE ABNORMALITIES ■ AZOTEMIA

Small Animal The Compendium November 1996

consistent development than

Physical examination findings and routine laboratory is icterus in cases of pomona
test results are consistent with leptospirosis. and grippotyphosa infection.2
Urinalysis is usually ab-
normal in cases of acute re-
Initiate therapy immediately—
nal leptospirosis and reflects
do not wait for confirmatory test results.
tubule damage rather than
glomerular disease. Exami-
nation of urine sediment re-
INITIAL THERAPY DIAGNOSIS veals erythrocytes and white
blood cells. Granular casts
• Place intravenous • Submit serum sample are inconsistently present.
catheter and initiate for microscopic agglu- Casts are more likely to be
diuresis. tination test for lepto- observed if the samples are
• Begin penicillin therapy spiral antibody titers. processed rapidly because
(see text for adjust- • Submit freshly collected casts break down over time.
ment). urine sample for dark- Urine specific gravity may
• Monitor urine output field microscopy, if be isosthenuric or mildly
and central venous available.
concentrated. More than
pressure. • Obtain kidney biopsy
half of the dogs infected
• Assess coagulation specimens; request
with pomona or grippoty-
status and correct special staining tech-
abnormalities. niques for identification phosa had glucosuria. In the
• Monitor blood urea of leptospires. absence of concurrent hy-
nitrogen, creatinine, • Acute titer greater than perglycemia, glucosuria is
and electrolytes. 1:800 supports the pre- indicative of acute insult to
• Consider colloid or plas- sumptive diagnosis; ob- renal tubules.
ma therapy if patient is tain convalescent titer Glomerular protein leak-
hypoalbuminemic. in 2 to 4 weeks for con- age is not typically present.
• Initiate parenteral firmation. Color changes detected by
or enteral nutritional • If acute titer is less than urine dipstick may result
therapy if patient is 1:800, contact refer- from darkening of the re-
anorectic. ence laboratory and a gent strip by increased
consider fluorescent numbers of red and white
ON RECOVERY antibody techniques, blood cells rather than pro-
enzyme-linked im- tein.
• Begin oral doxycycline munosorbent assay Leptospires are not de-
therapy (ELISA) antibody titer, tected in routine microscop-
• Educate owner about polymerase chain reac- ic examination of urine sed-
protection from zoonotic tion assay, or culture of iment because the
infection: organism; obtain conva- organisms cannot be stained
• Wear latex gloves lescent titer in 2 to 4 with typical dyes. 22 Dark-
when handling urine. weeks.
• Clean urine-soiled field microscopy of freshly
areas with iodine- collected urine is required to
based disinfectant. visualize leptospires during
• See family physician renal shedding. However,
if any humans in darkfield microscopy is of-
household become ten unrewarding because
ill. shedding can be intermit-
tent.4 Some laboratories can
perform fluorescent anti-
body identification of lep-
tospires in urine, but this
Figure 2—Diagnosis and management of acute renal failure due to leptospirosis.
procedure is not serovar-

URINE SEDIMENT ■ CASTS ■ DARKFIELD MICROSCOPY

Small Animal The Compendium November 1996

specific.14 Routine bacterial oratory findings are com-

culture of urine will not yield patible. 14 A convalescent
leptospires but may yield titer that does not change
other bacteria if the dog has from the acute sample sug-
a concomitant infection. gests previous or inactive
In the kidneys, typical infection.
histopathologic lesions due Several aspects of micro-
to pomona or grippotyphosa scopic agglutination sero-
infection consist of lympho- logic testing are important
plasmacytic and neutrophilic in making an accurate di-
tubulointerstitial nephritis agnosis. Cross-reactivity
(Figure 3A). Lesions can be against multiple serovars
mild to severe. Leptospires often results in increased
are occasionally seen within titers against several sero-
renal tubules after Warthin- Figure 3A vars during the acute phase
Starry staining, silver im- of the disease. The serovar
pregnation, or fluorescent eliciting the highest titer is
antibody techniques (Figure usually considered to be the
3B). Because the organisms infecting agent; lower titers
are not always present in are attributed to cross-reac-
biopsy samples, histopatho- tivity.14 Titers against a single
logic signs of inflammatory serovar usually predominate
interstitial nephritis should on convalescent samples.4,5
prompt further diagnostic This is probably due to the
testing for leptospirosis. development of homolo-
gous antibodies.31 Also, nat-
DIAGNOSIS urally occurring or stimu-
Leptospirosis is usually a lated immunity against
serologic diagnosis because leptospires is serovar-specif-
the organisms are difficult to ic. Vaccinated dogs may
Figure 3B
cultivate in the laboratory therefore have titers against
and are inconsistently de- Figure 3—Photomicrographs of renal tissue from a dog with canicola and icterohaemor-
tected in histopathologic or acute renal failure due to leptospirosis. (A) The renal corti- rhagiae. Usually, titers are
urine samples. The micro- cal interstitium is infiltrated and expanded by lymphocytes negative or below 1:320 and
scopic agglutination test and plasma cells (H&E; original magnification ×1000). persist for a few months af-
(B) Small spirochetes (black) within an epithelial cell of a ter vaccination.32,33 Howev-
(MAT) is the most widely
proximal tubule (modified Steiner’s stain; original magnifica-
used method of determining tion ×3300). (Courtesy of Stephen D. Lenz, DVM, PhD, er, postvaccination titers can
anti-Leptospira antibody College of Veterinary Medicine, Auburn University) be as high as 1:1250.4,34
29
titers. Live leptospires Because of the possibili-
grown in liquid media are ties of high postvaccination
exposed to serial dilution of titers and cross-reactivity, it
patient sera. Antibody in patient serum causes aggluti- has been suggested that only titers greater than 1:3250
nation of the organism. The reported titer against a should be considered diagnostic.2,5 If the dog was vacci-
particular serovar reflects the highest serum dilution nated more than 3 months previously, however, an anti-
that will cause 50% of the serovar to agglutinate. The body titer of 1:800 to 1:1600 is presumptive evidence of
microscopic agglutination test does not distinguish be- leptospiral infection.14
tween classes of immunoglobulins, although both IgG Microscopic agglutination titers may be negative
and IgM can cause agglutination of organisms.30 during the first week of infection.22 After infection and
Demonstration of at least a fourfold increase in anti- recovery, antibody titers usually decline gradually but
body titer 2 to 4 weeks apart is the most definitive sero- may persist for months.14 Early antibiotic therapy or
logic means of diagnosing leptospirosis. In general, a corticosteroid administration may inhibit convalescent
single high titer (≥1:800) is sufficient for a diagnosis of titers.
leptospirosis if the patient’s history and clinical and lab- Enzyme-linked immunosorbent assays (ELISAs) that

SEROLOGY ■ CROSS-REACTIVITY ■ POSTVACCINATION TITERS

Small Animal
can distinguish between IgM and IgG anti-Leptospira
antibodies have been developed. These tests can be
helpful when the microscopic agglutination test yields
confusing results. Dogs reliably develop an elevated
IgM titer greater than 1:320 in the acute phase of lepto-
spirosis.35 The proportion of IgM and IgG antibodies in
the convalescent phase after experimental immuno-
stimulation varies depending on the serovar.30
Polymerase chain reaction (PCR) assay of leptospiral
DNA is an effective means of diagnosing infection be-
fore an antibody titer develops or when titers are low
and the clinical course confusing.36–38 Most veterinary
laboratories only offer the microscopic agglutination
test. Few attempt bacterial culture of leptospires.
Special requests for ELISA, fluorescent antibody
techniques, polymerase chain reaction, or isolation of
leptospires from biological samples can be made by
contacting a referral or state diagnostic laboratory.
TREATMENT
Antibiotic Therapy
Treatment of leptospirosis consists of antibiotic ther-
apy and supportive care—regardless of the infecting
serovar. Two phases of antibiotic therapy are recom-
mended to decrease leptospiral replication, limit lep-
tospiremia, and shorten the phase of urine shedding.
Penicillin is the antibiotic of choice for treatment of
leptospiremia and should be administered early in the
course of the disease. Penicillin G procaine (40,000 to
80,000 U/kg intramuscularly or subcutaneously every
24 hours or divided every 12 hours) is the form of
penicillin most commonly used for treatment of lepto-
spirosis, although ampicillin and amoxicillin may also
be effective.1,39
Because penicillins are eliminated primarily via the
renal tubules, the dose should be adjusted for patients
with azotemia: Either the dose should be divided by
four, or the dose interval should be multiplied by
four.40 These adjustments are based on estimates of
decreased glomerular filtration rate and should be fol-
lowed until azotemia resolves. Penicillin therapy should
be initiated before the results of serology tests are re-
ceived and should be continued for 2 weeks or until
azotemia resolves.1
Doxycycline (2.5 to 5 mg/kg orally every 24 hours
for 2 weeks) is recommended after the conclusion of
penicillin therapy to eliminate leptospires from the kid-
ney. Dihydrostreptomycin and tetracycline have also
been recommended for this purpose. These drugs,
however, have nephrotoxic effects in patients with renal
disease. Doxycycline is eliminated via the intestine and
has been shown to be effective against leptospirosis in
humans.41
PENICILLIN ■ DOSE ADJUSTMENT ■ DOXYCYCLINE
The Compendium November 1996
Supportive Care
Supportive care measures for patients with lep-
tospirosis are directed at the affected organ systems.
Moderately to severely affected patients are usually
dehydrated and require intravenous fluid-replacement
therapy with a balanced electrolyte solution (e.g., lac-
tated Ringer’s solution). Animals in acute renal failure
require intravenous volume expansion to increase renal
blood flow and initiate diuresis.42 Placement of a jugu-
lar catheter will allow fluid administration, frequent
blood sampling, and measurement of central venous
pressure.
Urine output should be greater than 2 ml/kg/hr. Ani-
mals producing inadequate urine volumes after volume
expansion may benefit from administration of manni-
tol, diuretics, or dopamine.42 When oliguria or anuria
persists despite medical therapy, peritoneal dialysis
should be considered. Peritoneal dialysis is an expensive
and labor-intensive intervention best reserved for re-
versible causes of renal failure.42
Acute renal failure due to leptospirosis is usually re-
versible. Renal biopsy findings indicating tubule regen-
eration and an intact basement membrane are compati-
ble with reversible lesions. Other abnormalities that
may require specific therapy include electrolyte imbal-
ances, metabolic acidosis, hyperphosphatemia, vomit-
ing, and gastrointestinal ulceration.42
Thrombocytopenia and vasculitis, though often tran-
sient, may predispose patients to disseminated intravas-
cular coagulation and bleeding. Replacement therapy
with whole blood or plasma is indicated if patients have
coagulation disorders with or without active bleeding.43
Fibrinogen, fibrin degradation product, prothrombin
time, and partial thromboplastin time may reveal sub-
clinical coagulation disorders and should be evaluated
before renal biopsy is performed.
The dilutional effects of fluid therapy may exacerbate
hypoalbuminemia. Hypoalbuminemia may predispose a
patient to pulmonary or systemic edema. Administra-
tion of plasma or colloids will increase plasma oncotic
pressure and protect against the formation of edema.44,45
Parenteral or enteral nutritional supplementation may
hasten recovery from hypoalbuminemia by providing
amino acids necessary for protein synthesis.46,47
Recovery from leptospirosis is associated with resolu-
tion of azotemia and other hematologic and biochemi-
cal abnormalities and improvement in the patient’s atti-
tude and appetite. Dogs that recover from leptospirosis
may have permanent renal damage and develop chronic
renal disease. Usually, renal function and clinical im-
provement are adequate, and animals are discharged
from the hospital. Renal function should be assessed for
several months after recovery—regardless of the initial
Small Animal
response to therapy. Monitoring for systemic complica-
tions of chronic renal failure (e.g., hypertension, gas-
trointestinal ulceration, vomiting, hypokalemia, and
hyperphosphatemia) is also warranted.
ZOONOSIS
Of 191 reported human cases of leptospirosis, 31%
involved contact with rats and 30% involved contact
with dogs.48 Human cases of leptospirosis contracted
from dogs are sporadic but have involved veterinarians
exposed at work.23–25 During the past two decades, 50
to 100 human cases of leptospirosis per year were re-
ported to the Centers for Disease Control and Preven-
tion (CDC).49 Leptospirosis has not been targeted for
eradication because of its low human fatality rate.
Moreover, the organism is invulnerable to eradication
because of extensive domestic and wild animal reser-
voirs and the existence of many serovars.7 In 1995, the
CDC removed leptospirosis from the list of nationally
notifiable diseases.
Urine is the most important source of leptospiral
contamination after acute infection. Veterinary clini-
cians and staff should wear protective latex gloves when
handling any dog with a possible case of leptospirosis.
Areas soiled by the dog’s urine should be cleaned with
an iodine-based disinfectant; protective gloves should
be worn during cleaning.22 Leptospires may continue to
be shed in the urine for months despite clinical recov-
ery and an effective immune response.
VACCINATION
The commercially available vaccines for leptospirosis
contain inactivated bacterins of the serovars icterohaem-
orrhagiae and canicola. Vaccination is effective in reduc-
ing the severity of icterohaemorrhagiae and canicola
infection but does not prevent the carrier state.22 Vacci-
nation in dogs induces an IgG titer that subsides in ap-
proximately 3 months.33 Frequent vaccination in areas
where these serovars are enzootic is recommended. Pen-
tavalent vaccines containing antigens from the serovars
icterohaemorrhagiae, canicola, grippotyphosa, pomona, and
hardjo have provided antibody titers against all five
serovars for longer than 1 year.30 Whether such a vaccine
will be developed for veterinary use depends on the
commercial prospects for the vaccine.
About the Author
Dr. Wohl is affiliated with the Department of Small Animal
Surgery and Medicine, College of Veterinary Medicine,
Auburn University, Alabama. He is a Diplomate of the Ameri-
can College of Veterinary Internal Medicine and the Ameri-
can College of Veterinary Emergency and Critical Care.
URINE SHEDDING ■ DISINFECTANTS ■ PENTAVALENT VACCINE
The Compendium November 1996
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The Compendium November 1996
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