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International Journal of Aquaculture, 2014, Vol.4, No.24 1
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6
the possibility of increase in pH values during early
afternoon is inevitable coupled with the high
photosynthetic active radiation (PAR) and the
corresponding increase in photosynthetic uptake of
CO
2
due to the high abundance of phytoplankton
during the event which can reach up to 1.2 mg L
-1
of
Chl-
a
concentration (Teshome, 2011). This has
obvious consequence on the content of toxic gaseous
ammonia which is already above the optimum range
in the studied lakes for most tilapia species and
certainly increases further with rising pH during early
aftrnoon (El-Sherif, 2008).
Several studies have revealed different threshold
values for ammonia toxicity of tilapias. Popma and
Lovshin (1996) reported that acute toxicity and mass
mortality results when concentration of ammonia is
higher than 2 mg L
-1
although tilapia can survive up to
3 mg L
-1
of unionized ammonia concentration for few
days if slowly acclimatized; a case in many natural
water bodies. Therefore, the apparent high ammonia
concentration (2.1 mg L
-1
) is probably the overriding
factor which intoxicates the fish and subsequently
cased mass mortalities in Lake Babogaya. Apparently,
prolonged exposure to a concentration as high as 0.2
mg L
-1
can lead to mass mortality and a concentration
of 0.08 mg L
-1
(which is lower than the 0.1 mg L
-1
in
Lake Hora-Arsedi) can stress the fish there by
predisposing them to bacterial and parasitic infections
eventually causing mortalities (Benli et al, 2008).
Recent studies by El-Shafey (2008) indicated that
threshold values even as low as 0.05 mg L
-1
of total
ammonium (not the unionized form which should be
far lower than this value when calculated at a given
pH and temperature) can further stress tilapia species.
However, no comparative studies have been done so
far to the best of our knowledge on the ammonia
tolerance of the other species:
Tilapia zilli
and
Clarias
gariepinus
, which are considered to be resistant to
many diseases and environmental stress (Kirk, 1972).
Histopathological and bacteriological examinations
have shown that
O. niloticus
fish from both lakes were
infected by
Aeromonas
sp.
and
Plesimonas shigelloides
bacteria; and pericardial and gastro intestinal parasites
such
Contracaecum sp
.,
Clinostomum cutanum
and
Acanthocephalus sp
. Plumb (1997) found that
Aeromonas hydrophilia
infected fish as secondary
infection, whilst Al-Dughaym (2000) reported an
increased susceptibility of
O. niloticus
to
Aeromona
s
infections during an aquaria experiment with water
sources from infected natural water bodies compared
to controlled aquaria water. In this study, fish were
experimentally infected with
Aeromonas
isolated from
fish during mass mortality in which water from the
infected natural water contained significantly higher
stressive factors such as temperature, pH, alkalinity,
hardness and other nutrients. Indeed, a similar
scenario has been noted in lakes Babogaya and
Hora-Arsedi during the current mortality event as the
fish were stressed with elevated ammonia content
probably for several weeks which damaged the gills
and subsequently made the fish susceptible for
bacterial and parasitic infections. Furthermore,
O.
niloticus
fingerlings transported from L. Babogaya to
NFALRC ponds (for breeding and growth experiment)
exhibits similar mortality rates, while
T. zilli
fingerlings remained unaffected. Therefore, bacterial
and parasitic infection as a result of predisposition due
to water quality stress is the overriding and plausible
explanation to the current mortality of
O. niloticus
in
the Bishoftu crater lakes.
The possibility of algal toxicity from the dominant
bloom of
Microcystis aeruginosa
has been linked to
several mass fish kill events (see review by Singh and
Pathak, 2010; Adamovský, 2010), though the effect of
cyanotoxins on fish requires highly controlled
experiment and thus was not the purpose of this
snapshot survey. Nevertheless, live fish samples have
shown clinical symptoms such as liver and kidney
damage and hemorrhagic shock, similar to that of
cyanotoxin induced deaths (Adamovský, 2010), which
possibly also contributed to the current mortality
incident.
Concluding remark
The current catastrophic mass mortalities of
Oreochromis niloticus
in Lakes Babogaya and
Hora-Arsedi is caused by direct ammonia toxicity and
extended sublethal ammonia exposure and subsequent
stress induced bacterial and parasitic infection. In
addition, other possible factors such as cyanotoxin
should be further studied in these lakes. A further
comparative ammonia and disease tolerance study on
T. zilli
and
C. gariepinus
should explain why these
species were not affected by the current incident of
mass mortality although they are commonly believed to
be highly tolerant to disease and environmental stress.