Abstract
Peste des petits ruminants (PPR) isa major threat for small ruminant production in Bangladesh. Knowledge of pathogenesis helps to control disease but that is insufficient for PPR in Black
Bengal goats. The present study was aimed at elucidating the pathogenesis of PPR on
experimental infection. A total of eight Black Bengal goats were infected via intranasal route with
a field isolate of PPR virus (PPRV), which was isolated and characterized from a recent natural
outbreak using a newly developed goat kidney cells. Four goats were kept as uninfected control.
The infected goats were sacrificed at different days post infection (dpi). The responses of infected
and control goats were analyzed using clinical signs, gross and histopathology, hematological
and biochemical changes, virus distribution and localization and immune responses. Molecular
characterization revealed high genetic homology of the inoculum virus with other field isolates of
Bangladesh. All infected goats developed clinical signs typical for PPR. Based on clinical signs
and temporal distribution of the virus the course of PPR may be divided into four overlapping
phases: incubation (4-8 dpi), primary viremia (5-13 dpi), secondary viremia (8-13 dpi), and
convalescence or fatality (≥13 dpi). During the incubation period, the infected goats showed no
visible clinical signs. At the phase of primary viremia, infected goats developed dullness, clear
watery nasal and ocular discharges and rise of body temperature (104-105 °F). The second
viremic phase was similar to the primary viremic phase but with more severe clinical signs and
more rise of body temperature (>106 °F). At the 4th stage, 3 out of 8 infected goats died. Five goats
were sacrificed at different time points. With real time qRT-PCR the highest concentration of the
virus was found in trachea and pre-scapular lymph nodes at 5 dpi, in lungs at 7 dpi and
visceral organs and mucosa from 14 days onward. At necropsy, PPR infected goats showed
hemorrhagic spots and congestion in the respiratory, digestive and lymphoid organs which
usually aggravated with times. The affected lungs showed gradual consolidation. White to
at
grayish necrotic spots were found on the outer surface of liver. Kidneys were severely
hemorrhagic and inflamed. The major histopathological findings included hemorrhages,
congestion, mononuclear infiltration and extensive necrosis in the respiratory, digestive and
lymphoid organs where few cells contained viral inclusion bodies. Salivary glands were filled
with mucus. In the lungs severe infiltration of large mononuclear and giant cells affecting 70% of
the tissues and filling of alveolar lumens with exudates were found. In liver, at early stage fatty
change and single hepato-cellular necrosis occurred which later progressed to focal necrosis. In
kidney, necrotic tubules, fusions of tubular epithelia and hemorrhages with accumulation of
necrotic materials in tubular lumen were found. Hemorrhagic lesions in the intestine, lymphoid
necrosis and depletion in spleen and lymph nodes were observed. Immunohistochemistry
revealed localization of viral antigen in epithelial cells, lymphocytes and in antigen presenting cells of different visceral organs including liver and kidneys. On hematology, leukocytosis was
found at initial stages; however, leukopenia was developed from 7 dpi due to lymphopenia.
Biochemical analyses revealed all enzymes related to liver and kidney functions (ALT, AST,
alkaline phosphatase, creatine kinase, Urea B and BUN) and electrolytes (Na+& Cl-) increased significantly in PPR infected goats. Total protein and albumin decreased significantly. The ELISA showed that 100% infected goats developed anti-PPR antibody at 14 dpi. In conclusion, the pathogenesis of PPR is proposed as follows: viral entry through orinasal routes; primary viremia
and initial replication in the regional lymph nodes, followed by massive replication in the lungs
leading to secondary viremia and subsequent distribution in other visceral organs and mucosa
with massive tissue damage. Diarrhea developed during or after the second viremic phase and
majority of the infected goats died due to dehydration, kidney and respiratory dysfunction.
Further studies should focus on more detailed studies on the molecular and cellular responses of
the host to PPR virus infection