South Africa. Ante-mortem diagnosis is very difficult.
Intradermal tuberculin testing is unreliable in
rhinos. Tracheobronchial and gastric lavage samples
can be used for mycobacterial culture. Serology
appears promising and there are some commercial
kits available (Chembio VetTB DPP). Research on
experimental cytokine assays is underway. Most
diagnoses are made post-mortem, however.
Paratuberculosis (M. avium subsp. paratuberculosis)
– This has been diagnosed in a single captive black
rhino. The animal had a 4 month history of diarrhoea
and weight loss. M. avium subsp. paratuberculosis
was isolated from a faecal culture. The rhino was
treated with anti-mycobacterial drugs and clinically
Leptospirosis – This is a zoonotic disease with
worldwide distribution. Leptospirosis is caused by one
of more than 250 pathogenic serovars of Leptospira.
Rodents are the maintenance hosts. Antibodies
have been reported in wild black and white rhinos
in range countries. Urine-contaminated feed is the
source of infection. Transmission occurs through
contact of the bacteria with mucous membranes
or damaged skin. Leptospires can colonize the liver,
kidneys, lungs, genital tract, and CNS. Clinical signs
are variable; acute, systemic febrile disease with renal
and/or hepatic damage has been reported in black
rhinos; uveitis, haemolytic anaemia, muscle pain, and
abortion/stillbirth may also occur. Leptospirosis can
be confirmed by identifying bacteria in blood, urine
or tissues using immunofluorescence, PCR, or culture;
however, it is more commonly diagnosed by elevated
antibody titres using a microagglutination test. A
4-fold increase in serum samples taken 7-10 days
apart or a single titre>1:800-1600 with compatible
clinical signs are common criteria. Prevention
includes good rodent control and vaccination using a
polyvalent inactivated vaccine.
Clostridial diseases – C. septicum: Malignant oedema
occurs when there is bacterial contamination of
wounds with local toxins causing severe oedema and
necrosis. This disease may be a concern for rhinos if
there is fighting, transport, or other wounds.
C. tetani: There are rare cases of tetanus in rhinos
associated with spore-contaminated wounds. Clinical
signs are similar to those in domestic animals. Equine
tetanus vaccine has been used in captive rhinos.
C. sordelli: There has been a fatal outbreak in white
and black rhinos under semi-intensive management.
Presented with peracute sig ns; typically animals
would collapse and progress rapidly to death. On post-
mortem, haemorrhagic enterocolitis was evident. A
vaccine has been developed.
C. perfringens (Enterotoxaemia): This has resulted in
9 black rhino mortalities in Kenya, as well as morbidity
in captive black and white rhinos. Clinical signs are
often peracute with severe abdominal pain, laboured
breathing, and death within hours. Severe necrotizing
haemorrhagic enteritis is found at necropsy.
Overgrowth of intestinal flora can be precipitated by
change in diet, stress, and antibiotic treatment.
Diagnosis of clostridial diseases usually requires
anaerobic culture of gastric or small intestinal
contents, or tissue (including wounds). There are PCR
assays for toxin genes. A mouse bioassay can also
be used to detect toxins. Histopathology provides
Treatment requires intensive supportive care and
potential administration of antitoxin if diagnosed
early. Prevention is the key and there are multivalent
vaccines that have been used in rhinos.
Streptococcal and Staphylococcal Infections – Beta-
haemolytic Streptococcus has been isolated from
skin lesions and wounds in rhinos; this may progress
to septicaemia and death. It has also been linked to
vegetative endocarditis, myocardial degeneration,
meningoencephalitis, and Idiopathic Haemorrhagic
Vasculopathy Syndrome in captive black rhinos.
Methicillin-resistant Staphylococcus aureus (MRSA)
has been isolated from chronic wounds on captive
rhino feet (zoonotic threat).
Encephalomyocarditis virus (EMCV) – Typically a
peracute disease with signs consistent with cardiac
failure. Non-suppurative myocarditis and pulmonary
oedema found post-mortem. Survivors may have
cardiac damage. Exposure is measured by antibody
titres, with diagnosis confirmed using virus culture,