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→Clinical Signs
*Giant cells may be seen in the alveol
*Giant cells may be seen in the alveol
===Clinical Signs===
===Clinical Signs===
First clinical signs are characterized by lethargy,
dehydration, anorexia, and weight loss followed by a more
pronounced clinical manifestation depending on the predominantly
affected organ. Development of a biphasic fever
represents another characteristic clinical finding (Wright
et al., 1974). A transient fever and the onset of lymphopenia
can be observed 3–6 days pi (Krakowka et al., 1980) and
coincide with the first viremia that results in a generalized
infection of all lymphoid tissues including spleen, thymus,
lymph nodes, bone marrow, mucosa-associated lymphatic
tissues(MALT) and macrophages in the lamina propria of the
gastrointestinal tract (Appel, 1970; Wright et al., 1974), as
well as hepatic Kupffer cells (Appel, 1987). Viremia occurs
by spread of cell free virus as well as leukocyte and
thrombocyte associated infectious pathogens. The second
viremia follows several days later, frequently associated
with high fever, and results in infection of parenchymal and
tissue cells throughout the body (Appel, 1969; Appel and
Gillespie, 1972; Blixenkrone-Møller, 1989; Blixenkrone-
Møller et al., 1989; Okita et al., 1997). Thus, CDV can be
found in cells of the respiratory, gastrointestinal and urinary
tract, endocrine system, lymphoid tissues, central nervous
systemand vasculature including keratinocytes, fibroblasts,
thrombocytes and different lymphoid cell subsets, aswell as
bronchial, endothelial, epithelial and neuroectodermal cells
(Baumga¨ rtner et al., 1989; Gro¨ne et al., 2004a,b; Koutinas
et al., 2004).
5.2. Clinical manifestations
According to clinical features a catarrhal and nervous
form or a combination of both, also termed acute systemic
form, and a chronic nervous manifestation can be distinguished.
In addition, various unusual manifestations,
including old dog encephalitis and hard pad disease are
recognized (Krakowka et al., 1985; Baumga¨ rtner, 1993;
Moritz et al., 1998, 2000, 2003). At the acute stage, virus is
found in every secretion and excretion of the body. This
phase is accompanied by various dramatic clinical signs
including onset of a cutaneous rash, serous nasal and ocular
discharge, conjunctivitis and anorexia, followed by gastrointestinal
and respiratory signs, which are often complicated
by secondary bacterial infections and neurological
disturbances (Krakowka et al., 1985). Nervous signs are
diverse and progressive (Parker, 1978; Greene and Appel,
1998) and include myoclonus, nystagmus, ataxia, postural
reaction deficits and tetraparesis or plegia (Koutinas et al.,
2002; Vandevelde and Zurbriggen, 2005; Amude et al.,
2007).
In some cases, an improved immune response especially
an increased production of virus-specific neutralizing
antibodies can promote the recovery of the animal.
However, despite elimination of the virus from several
organs and the peripheral blood, CDV can persist in certain
tissues including uvea, CNS, lymphoid organs and footpads
(Appel, 1970, 1987; Zurbriggen et al., 1995a,b; Greene and
Appel, 1998; Gro¨ne et al., 2003a; Schobesberger et al.,
2005). Moreover, some infected animals display a delayed
progression of the disease and a moderate immune
response with subtle early clinical signs. Later, as a
consequence of viral persistence in the CNS, overt CNS
disturbances can be observed resulting in the nervous form
of canine distemper. Dogs with nervous signs usually die,
but some recover, and may display lifelong residual signs
such as a persistent myoclonus.
Canine distemper is usually an acute, febrile disease, especially of young dogs, although older unprotected dogs are also susceptible. The first clinical manifestation of distemper is a diphasic febrile response. The first response may be overlooked, but the second generally occurs 2 - 3 days later in conjunction with other clinical signs, which initially include congested conjunctiva and nasal mucosa with subsequent serous to mucopurulent discharges. Pneumonia, depression, anorexia, vomiting, and diarrhea usually follow. Neurologic disturbances, such as neuromuscular tics, "chewing gum" seizures, and paresis are frequent sequelae in dogs that recover from acute disease.
Canine distemper is usually an acute, febrile disease, especially of young dogs, although older unprotected dogs are also susceptible. The first clinical manifestation of distemper is a diphasic febrile response. The first response may be overlooked, but the second generally occurs 2 - 3 days later in conjunction with other clinical signs, which initially include congested conjunctiva and nasal mucosa with subsequent serous to mucopurulent discharges. Pneumonia, depression, anorexia, vomiting, and diarrhea usually follow. Neurologic disturbances, such as neuromuscular tics, "chewing gum" seizures, and paresis are frequent sequelae in dogs that recover from acute disease.
Hyperkeratosis of the nose and digital pads ("hard pad") develops in some cases. Pustular dermatitis may be seen affecting the abdomen of puppies.
Hyperkeratosis of the nose and digital pads ("hard pad") develops in some cases. Pustular dermatitis may be seen affecting the abdomen of puppies.