Update on Zoonosis--I: Tuberculosis & Herpesvirosis
World Small Animal Veterinary Association World Congress Proceedings, 2009
José Luiz Catão-Dias, DVM, MSc, PhD
Associate Professor of Comparative Pathology Department of Pathology, Faculty of Veterinary Medicine and Zootechny (FMVZ), University of São Paulo (USP), São Paulo, Brazil

The present lectures aim to address the major aspects related to tuberculosis, herpesvirosis, yellow fever and leishmaniasis. The main aspects of these diseases are briefly reviewed, with special emphasis on their respective dissemination patterns, zoonotic characteristics, and preventive measures.


Tuberculosis (TB) is a chronic, granulomatous, debilitating, and highly infectious-contagious disease caused by slow-growing bacteria that belongs to the Mycobacterium tuberculosis-bovis complex.1,2 The disease affects a wide range of vertebrates and is of high public health concern. The characteristics of TB vary according to the species of the host, the route of infection, the dose of the inoculum, the virulence of the pathogen, and the host-pathogen relationship that further establishes.1,2 Concerning wild animals, TB is a disease commonly observed among captive animals, and rarely is found in their free-ranging counterparts. For the latter, it usually occurs when free-ranging wild animals exhibit close or direct contact with human beings.1 However, it is important to mention that a number of recently reported situations of TB has been associated with relevant impact on a variety of free-ranging animals, such as bovids, cervids, great apes and marine mammals.1

Mycobacteria are facultative or obligate intracellular bacilli. Although presenting a cellular wall compatible with gram-positive bacteria, Mycobacteria are not permeable to dyes used in this technique due to their elevated lipidic concentration.1 On the other hand, histologic methods using their alcohol-acid resistance characteristics are commonly used to detect the pathogen.1,2

Infection occurs predominantly after mycobacteria ingestion or inhalation. Other infection routes, including transplacentary and transcutaneous, are also described. Infected animals may eliminate the pathogen on respiratory discharges, submandibular fistulas, feces, and urine.1,2 Clinical signs vary according to affected species. However, sick animals usually show fever, anorexia, and weight loss. Other abnormalities commonly associated with TB are respiratory and/or digestive dysfunctions, including cough, dyspnea, dysphagia, tonsillar enlargement, diarrhea and vomiting.1,2,3 Gross lesions found are characterized by granuloma formation. The size, location, extension, and dissemination pattern of the granuloma depend on several factors related to the host-pathogen relationship that is established.1 Microscopically, the granuloma is characterized by its cellular components and the presence or absence of caseous necrosis.1,2 Anti-mortem diagnosis of TB in exotic animals is an issue of major challenge. The isolation of mycobacteria is considered the gold standard for the diagnosis. Clinical laboratory findings are usually non-specific, as are the radiographic exams. Tuberculin testing frequently presents inconclusive results.1,2,3 Recently, diagnostic tools based on antibody detection have been developed with promising perspectives for some non-domestic species. Treatment, when applicable, demands the association of multiple drugs, simultaneously administered. Isoniazid, rifampicin, ethambutol, pyrazinamide, and dihydrostreptomycin are among the antimicrobial drugs of choice.1,2,3 Mycobacteria are among the most resistant organisms to disinfection. They are highly resistant to environmental conditions, including elevated temperatures and ultra-violet light. Disinfection success depends on the chemical substances used and their relative concentrations, methods of application, presence of organic matter, and duration of effective contact between the disinfectant and the pathogen.2,3


Herpesvirosis is the generic denomination given to the diseases caused by a number of related viruses of the family Herpesviridae, which is further divided into the sub-families Alphaherpesvirinae, Betaherpesvirinae, Gammaherpesvirinae, and an unassigned one.1 The herpesviruses are double-stranded DNA viruses that share similar morphological and other infectivity characteristics.1,2 They cause destruction of reticuloendothelial and epithelial cells for replication, in varying degrees of severity. The course of infection is followed by establishment of latency in nervous ganglia.1 Latent herpesviruses can reactivate and thus present recurrent pathogenic effects on their hosts. Host immunity status and environmental factors are involved in the severity of herpesvirosis and recurrence episodes.1,2

A broad range of vertebrate species is susceptible to infections with herpesviruses.1 In most cases, each host species presents its own herpesviruses and the gravity of disease is usually low. Given this, it can be argued that species-specific herpesviruses might have co-evolved with their natural hosts. Latency followed by asymptomatic infection is also a common situation observed when such species-specific infections occur, and development of associated disease due to recurrence is a rare event. On the other hand, when a given herpesvirus crosses the barrier of its natural hosts and infects a different host species, a serious disseminated viral infection with a number of different clinical outcomes may occur.2

Here, emphasis is given to herpesviroses originated from non-human primates, especially those related to Cercopithecine herpesvirus 1 (CeHV-1).

The CeHV-1, formelly called Herpesvirus simiae, Herpesvirus B and B-virus, belongs to the sub-family Alphaherpesvirinae, genus Simplexvirus, and is related to Ateline herpesvirus 1, Cercopithecine herpesvirus 16, Saimirine herpesvirus 1, Human herpesvirus 1 and Human herpesvirus 2.3 The CeHV-1 is a common pathogen of the macaques of the genus Macaca (M. mulata, M. radiate, M. fuscata, M. arctoides, M. cyclopis, and M. fascicularis), and it is usually causative of asymptomatic infections in these hosts.1

Among natural hosts, CeHV-1 infection rates increase quickly with sexual maturity, reaching up to 90% of some colonies. The virus is transmitted by sexual activity and/or aggressive behavior, and occasionally, by fomites.1,4 Infection is for life and the virus may be shed sporadically through oral and/or genital secretions. Acute and disseminated disease in Macaca is rare. However, in special circumstances, mainly due to immunosuppression, affected macaques may develop fatal severe pulmonary, hepatic, lymphoid and central nervous system pathologic manifestations.1,4

In humans, CeHV-1 infection is a major concern among professionals dealing with non-human primates, especially macaques, and the number of human cases of infections has increased since 1987.1,2 Human infection is mainly associated with macaque-induced injury, but reports of cases due to respiratory transmission, professional exposure, and needle stick injury have also been documented.4,5 Clinical signs include vesicular dermatitis at the site of inoculation, followed by lymphangitis and disseminated lymphadenopathy. Cutaneous signs are followed by neurological manifestations, including ascending paralysis, paresthesia and disseminated encephalitis. Death occurs in approximately 70% of the cases.2

Prevention of human infection is mainly based on avoiding macaques-induced injuries and special attention when handling tissue samples. In case of exposure, intensive wound cleaning with water and soap for at least 10 minutes is recommended. Antivirals, as acyclovir and ganciclovir, may be used under close medical monitoring.2,4,5



1.  Catão-DiaS JL, Carvalho VM. Tuberculose. In: Cubas ZS, Silva JCR, Catão-Dias JL. (Eds) Tratado De Animais Selvagens: Medicina Veterinária. Ed. Roca. São Paulo. P.p. 726-735. 2007.

2.  Lack EE, Connor DH. Tuberculosis. In: Connor DH, Chandler FW, Schwartz DA, Manz HJ, Lack EE. (Eds) Pathology of Infectious Diseases. Appleton & Lange, Stamford. P.p.857-868. 1997.

3.  Gibson SV. Bacterial and mycotic diseases. In: Bennett BT, Abee CR, Henrickson R. Nonhuman Primates in Biomedical Research: Diseases. Academic Press, San Diego. P.p. 59-110. 1998.


1.  Mansfield K, King N. Viral diseases. In: Bennett BT, Abee CR, Henrickson R. Nonhuman Primates in Biomedical Research: Diseases. Academic Press, San Diego. P.p. 1-58. 1998.

2.  Schiffer SPB Virus infection--Infection by Cercopithecine herpesvirus 1. In: Connor DH, Chandler FW, Schwartz DA, Manz HJ, Lack EE. (Eds) Pathology of Infectious Diseases. Appleton & Lange, Stamford. P.p.141-146. 1997.

3.  Fauquet CC, Mayo MA, Maniloff J, Desselberger U, Ball LA. Viral Taxonomy; Eight Report of the International Committee on Taxonomy of Virus. Elsevier, Amsterdam. 1259p. 2005.

4.  Weigler BJ. Clin Infec Dis. 14: 555-567, 1992.

5.  Holmes GP, et al. Clin Infec Dis. 20: 421-439, 1995.


Speaker Information
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José Luiz Catao-Dias, DVM, MSc, PhD
Department of Pathology – Faculty of Veterinary Medicine and Zootechny (FMVZ)
University of São Paulo (USP)
Sao Paulo, Brazil

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