Chapter 28: Cyanobacterial poisoning in 

livestock, wild mammals and birds – an overview 

Ian Stewart1,2, Alan A. Seawright1, Glen R. Shaw2,3

1

: National Research Centre for Environmental Toxicology, University of 

Queensland, Brisbane, Australia; 2

: Cooperative Research Centre for Water 

Quality and Treatment, Adelaide, Australia; 3

: School of Public Health, 

Griffith University, Brisbane, Australia 

Abstract 

Poisoning of livestock by toxic cyanobacteria was first reported in the 19th

century, and throughout the 20th century cyanobacteria–related poisonings 

of livestock and wildlife in all continents have been described. Some mass 

mortality events involving unrelated fauna in prehistoric times have also 

been attributed to cyanotoxin poisoning; if correct, this serves as a reminder that toxic cyanobacteria blooms predate anthropogenic manipulation of the environment, though there is probably general agreement that 

human intervention has led to increases in the frequency and extent of 

cyanobacteria blooms. Many of the early reports of cyanobacteria poisoning were anecdotal and circumstantial, albeit with good descriptions of the 

appearance and behaviour of cyanobacteria blooms that preceded or coincided with illness and death in exposed animals. Early necropsy findings 

of hepatotoxicity were subsequently confirmed by experimental investigations. More recent reports supplement clinical and post–mortem findings 

with investigative chemistry techniques to identify cyanotoxins in stomach 

contents and tissue fluids. 
614 I. Stewart et al. 

Introduction 

Planktonic blooms and surface scums appear to have been recognised for 

over two thousand years, and indigenous peoples of North America, Africa 

and Australia may have been aware of the poisonous nature of cyanobacteria (Codd et al. 2005). Detailed studies – including microscopy – of the 

behaviour of planktonic cyanobacteria blooms began in the late 19th century. Surface scums that were concentrated by wind activity were observed, having a sudden onset and dissipation (Phillips, 1884). The world’s 

first scientific report of the toxic nature of cyanobacteria was written by 

George Francis, who described in 1878 the rapid death of stock animals at 

Lake Alexandrina, a freshwater lake at the mouth of the Murray River in 

South Australia (Francis 1878). Francis described a wind–blown surface 

scum of the brackish water cyanobacterium Nodularia spumigena, incidental consumption of which resulted in the death of sheep, horses, dogs and 

pigs within periods of 1 to 24 hours. Francis also experimentally dosed a 

sheep with fresh bloom material. Necropsy examination showed a significant pericardial effusion, “two pints of yellow serum” (i.e. most likely ascitic fluid) in the abdominal cavity, and normal–looking liver, lungs and 

kidneys (Francis 1878). Codd et al (1994) note that the observations of 

Francis are entirely in agreement with the modern understanding of Nodularia–associated intoxication through its associated cyanotoxin, nodularin. 

Beasley et al (1989a, 1989b) suggest that another cyanotoxin may have 

been involved, given that Francis did not report any hepatic pathology 

characteristic of nodularin intoxication, however the liver lesion caused by 

nodularin may not have been apparent or obvious to the inexperienced observer. The description of ascitic fluid in this context is strongly suggestive 

of acute liver damage. Beyond Francis’s (likely) observation of ascitic 

fluid, and the necropsy findings of (possibly) a single animal, it is probably 

unwise to attempt a reinterpretation of Francis’s findings (Francis did report opening “many sheep that died”, but it is not clear from the report 

whether his examinations of those field deaths extended beyond his obvious interest in the apparent absence of bloom material from the stomachs) 

(Francis 1878). 

Since Francis’s report in the last quarter of the 19th century there have 

been numerous descriptions of mammal and bird mortalities associated 

with exposure to cyanobacteria. The relevant literature throughout the 20th

century represents all inhabited continents. Anecdotal and case reports 

have been collated and/or reviewed by many authors, e.g. (Schwimmer and 

Schwimmer 1955, 1968; Schwimmer and Schwimmer 1964; Hammer 

1968; Codd and Beattie 1991; Carmichael and Falconer 1993; Ressom et 
Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds 615

al. 1994; Duy et al. 2000; Briand et al. 2003; Codd et al. 2005; Falconer 

2005). Many of the earlier reports are circumstantial, noting a temporal association between the presence of cyanobacterial blooms in a waterbody 

and otherwise unexplained mortalities. Early necropsy findings of hepatotoxicity were subsequently confirmed by experimental toxicology studies 

into isolated and purified cyanotoxins. More recent reports supplement 

clinical and post–mortem findings with investigative chemistry techniques 

to identify cyanotoxins in stomach contents and organs. 

Discussion of wild and domestic animal poisonings can be found in 

most reviews of toxic cyanobacteria, and mention of field deaths often 

served to introduce and contextualise reports of experimental toxicological 

investigations into cyanobacterial suspensions, extracts or isolates. As the 

number of primary anecdotal and case reports and reviews into cyanobacteria–related mortality of birds and terrestrial mammals is extensive, a systematic, comprehensive review has not been conducted in recent times. 

Such a task is also beyond the scope of this review; therefore we will present some selected discussion of early reports, including palaeontologic 

findings, then we will discuss more recent investigations that incorporate 

modern investigative chemistry techniques to supplement clinical and 

post–mortem findings in order to diagnose cyanotoxin poisoning. 

Early reports (pre–1960s) 

Lake Alexandrina in South Australia, as mentioned in the Introduction, 

was a trouble–spot for cyanobacteria–related poisonings, with several hundred deaths associated with a number of bloom events in the latter part of 

the 19th century. The local Aboriginal people were apparently aware of 

poisonings in the lake at around 1850 (Codd et al. 1994). 

Another early locus was South Africa, where Steyn (1945) suggested 

that “many thousands” of cattle and sheep mortalities over the preceding 

25–30 years were attributable to cyanobacterial poisoning; horses, mules, 

donkeys, dogs, hares, poultry and waterbirds found dead near affected waterbodies were also thought to be similarly affected. A toxic bloom on the 

Vaal Dam in 1942 covered an estimated 98 per cent of the reservoir, this 

being at the time 120km x 24km (at its broadest point) with a 1 teralitre 

capacity (Stephens 1949). Microcystis sp. were identified in the water; 

fulminant hepatic disease was observed in some animals, as were subacute 

cases with death ensuing after some two weeks and chronic cases with 

weeks or months of morbidity preceding either death or recovery. Necropsy findings in fulminant cases included pulmonary haemorrhage, hae-
61

moperitoneum, hepatomegaly (with livers dark red or black in colour, and 

friable), splenomegaly, and occasional “bloody patches...on the mucous 

membranes of [the stomach and intestines].” Findings in subacute cases 

were haemo–serous exudate in the pericardium, thorax and peritoneal cavity, the liver being soft or friable and yellow–coloured. Experimental dosing of animals with dam water produced identical clinical signs and post–

mortem lesions. Secondary photosensitivity was described in detail: painful inflammation, fissuring of affected epithelium, purulent discharge, 

sloughing of skin. Unpigmented areas are mainly affected – muzzle, udder 

and teats, ears (Steyn 1943). 

Cyanobacteria–related poisonings were reported in North America also 

from the latter half of the 19th century – see citations in Codd et al (2005). 

Howard and Berry (1933) discussed Anabaena–related cattle and other 

animal deaths at an Ontario lake in 1924. Storm Lake in Iowa experienced 

dramatic bloom events in 1952: associated with Anabaena flos–aquae 

blooms were estimated deaths of 5–7,000 gulls, 560 ducks, 400 coots, 200 

pheasants, 50 squirrels, 18 muskrats, 15 dogs, 4 cats, 2 hogs, 2 hawks, 1 

skunk, 1 mink, plus “numerous” songbirds. These figures were taken from 

the recorded number of animals buried by a field worker at the time, so 

were most probably underestimates of the total number of deaths. Signs of 

neurotoxicity were seen: prostration and convulsions preceded death; 

milder cases displayed restlessness, weakness, dyspnoea and tonic spasms. 

57 weak and partially paralysed mallards recovered following gastric lavage. A dog drinking the water when sick birds were being gathered then 

died near the lake shore when trying to escape from workers. Botulism was 

excluded from the diagnoses, and necropsy findings were unremarkable. 

Experimental oral or parenteral dosing of bloom filtrate to laboratory rodents and chickens resulted in rapid death – within minutes, though delayed mortalities were reported: one chicken lived for 48 hours, and guinea 

pigs exposed to bloom filtrate orally or by i.p. injection died “within 24 

hours” (Firkins 1953, Rose 1953). 

While some of the aforementioned reports were dramatic in terms of the 

number of animals affected by specific bloom events, equally compelling 

were early descriptions of the rapidity with which large animals succumbed after exposure to (presumably) neurotoxic cyanobacteria. McLeod 

and Bondar (1952) noted that a horse, “several” calves, two pigs and a cat 

all died within an hour of consuming cyanobacteria–affected water at Lake 

Dauphin, Manitoba in 1945. At the same site in 1951, nine dogs and a 

horse died within one hour; the horse showed signs of progressive muscular weakness and paralysis, with profuse sweating. Experimental dosing of 

laboratory rodents was conducted using bloom material (99% Aphanizomenon flos–aquae) collected from the lake six days after the last re6 I. Stewart et al. 
 617

ported poisoning event. Interestingly, oral or i.p. injections of lake water 

filtrate were not toxic, whereas unfiltered lake water, various preparations 

of cyanobacterial residue or filtrate from disrupted cellular material resulted in deaths ranging from under 12 hours to around 65 hours. Clinical 

signs were those of “loss of equilibrium followed by progressive paralysis.” Later signs were clonic muscular spasms and respiratory dysfunction 

leading to pronounced cyanosis. Post–mortem findings from these experimental animals were not reported (McLeod and Bondar 1952). 

Prehistoric animal mortalities 

The first detailed descriptions of the behaviour of cyanobacteria blooms 

and cyanobacterial toxicity were written in the latter part of the 19th century (see Introduction), but there is no reason to suppose that both phenomena were not present at earlier stages of our history. Codd et al (1994) 

suggest that Pliny the Elder may have described a cyanobacterial or algal 

scum on the River Dnieper in AD77, and Höger (2003) implies that an Old 

Testament reference may be a description of a piscicidal Planktothrix 

bloom in the River Nile. These contemporaneous descriptions reach modern researchers through the device of written language. However, two reports from the palaeontology literature suggest that cyanobacterial toxicity 

may be a prehistoric phenomenon. Braun and Pfeiffer (2002) present their 

hypothesis that at Neumark–Nord in Germany, a Pleistocene (1.8 million – 

11,000 years ago) lake assemblage of >70 deer, as well as forest elephant, 

rhinoceros, auroch (ox) and cave lion skeletons may represent a 

cyanotoxin–related mass mortality event. The preservation features and 

antler development suggest rapid, catastrophic death in autumn. Calcified 

layers in the sediment are thought to represent decomposed cyanobacteria, 

and absorption spectra of cyanobacteria–specific carotenoids were identified in sediment extracts. The authors used HPLC with UV detection to determine the presence of microcystins in methanol extracts of sediment; a 

similar (but not identical) UV spectrum to that obtained from an extract of 

a Microcystis aeruginosa strain with an unspecified microcystin congener 

profile was seen. Other possible explanations for the deaths at Neumark–

Nord – butchery by early humans, or a gas eruption – are discussed by the 

authors but thought to be unlikely (Braun and Pfeiffer 2002). Considering 

further the cyanotoxin hypothesis, it would be interesting to see further 

confirmatory investigations for microcystins in the sediment extracts using 

a second method such as mass spectrometry. Looking beyond the search 

for microcystins in the sediment, it would seem that sudden, catastrophic 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
618

death due to ingestion of a cyanobacterial neurotoxin could equally explain 

these events. 

An older mammal and bird assemblage from the Middle Eocene epoch 

(49 – 37 million years ago) also has features suggestive of a mass poisoning event. The Messel oil shale pit in Germany was an ancient freshwater 

lake. While the sediment layers are more compacted than those of Neumark–Nord, and chemical and physical transformation of sediments by 

diagenesis is likely, Koenigswald et al (2004) suggest that there are 

marked similarities across both sites, and thin layers of siderite at Messel 

probably represent the decomposed remains of sunken cyanobacteria 

blooms. Well–preserved skeletons of horses, turtles, bats and birds are 

found; most were in good health, and stomach contents show that they 

were well nourished. Apparent features of seasonal death are seen: of some 

50 dawn horse skeletons, five are of pregnant mares. The foetuses are all in 

late stages of development, which again suggests seasonal mortality, as 

predator pressure on newborn ungulates drives seasonal parturition, usually in late spring. These skeletons were found in different layers, so the 

picture is that of seasonal deaths occurring in different years. The frequent 

presence of winged animal skeletons at Messel, which is unusual in lake 

deposits, also supports a toxic waterbloom hypothesis (Koenigswald et al. 

2004). The authors also discuss a finding of aquatic turtle specimens in 

which two animals are preserved as pairs in close proximity to each other. 

“At least” five slabs of shale featuring such pairs of turtles have been 

found; photographs of two pairs are presented in the paper. The authors 

cite another worker’s interpretation of this finding as representing sudden 

death during mating, which would support a toxic cyanobacteria bloom 

hypothesis (Koenigswald et al. 2004). However the photographs show two 

pairs of turtles apparently fused posteriorly but facing away from each 

other, which is not the normal copulatory position adopted by turtles. The 

male mounts the female, though infrequent reports of “belly–to–belly” position can be found in the literature (Goode 1967, Kuchling 1999). 

If these reports do indeed describe ancient cyanobacteria–related intoxications, they serve as a reminder that toxic cyanobacteria blooms are natural events; they predate recent anthropogenic manipulation of the environment, and may indeed predate human arrival. However, most 

cyanobacteriologists would acknowledge that the problem of harmful 

cyanobacteria is exacerbated in modern times due to cultural eutrophication, and may worsen in future with the additional impact of human activity–related climate warming and other population–related pressures. 

 I. Stewart et al. 
 619

Recent developments 

While many early reports and reviews of cyanobacteria–related poisonings 

are impressive because of their comprehensive nature and empirical observations supplemented by simple experimental techniques, more recent reports of mammal and bird poisonings reveal the advances in analytical 

techniques that allow definitive identification of well–characterised 

cyanotoxins. The following section will present discussion of recent case 

studies that investigated animal poisonings caused – or likely to have been 

caused – by cyanobacteria that produce toxins from each of the main 

cyanotoxin groups that have been characterised to date. Clinical presentation, necropsy findings that reflect the current understanding of the mechanisms of toxicity, and modern investigative chemistry procedures that confirm the diagnosis are discussed. These examples are by no means 

exhaustive, as different analytical approaches may be applied, and factors 

such as dose, time period of exposure and ingestion of more than one type 

of cyanotoxin may complicate the diagnosis. 

The experimental toxicology of these isolated cyanotoxins has been well 

documented, and many excellent reviews are available, e.g. (Ressom et al. 

1994, Codd et al. 1999, Carmichael 2001, Falconer 2005). Peracute microcystin and nodularin poisoning presents principally with fulminant haemorrhagic liver injury; pathologic changes can also be seen in the gut, kidney, heart and lungs. Cylindrospermopsin intoxication is characterised by 

fatty degeneration of the liver, cholestasis, injury to renal tubules and 

thymic atrophy. Experimental dosing with cylindrospermopsin–producing 

cyanobacterial extracts results in pathological effects on other tissues and 

organ systems, including the gastrointestinal tract and spleen. 

Cyanobacterial neurotoxins cause death by respiratory failure through 

various mechanisms: anatoxin–a by a depolarising block at the neuromuscular junction; anatoxin–a(s) is an anticholinesterase, thus preventing the 

enzymatic degradation of acetylcholine which results in uncontrolled hyperstimulation of muscles. Hypersalivation and lacrimation, which are 

signs of parasympathetic stimulation, also characterise anatoxin–a(s) poisoning. The saxitoxin group are sodium channel blocking agents, thus interfering with axonal conduction. Death is very rapid – within minutes – 

when purified cyanobacterial neurotoxins are administered parenterally, 

particularly from anatoxin–a or saxitoxins. Post–mortem and histology 

findings are generally unremarkable. 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
62

Microcystins 

Case study: duck deaths in Japan, 1995 (Matsunaga et al. 1999) 

Shin–ike pond in Hyogo Prefecture had become eutrophic from the entry 

of untreated sewage following an earthquake in January 1995, when a 

sewage treatment plant was damaged. A bloom of M. aeruginosa was evident. In September of that year, some 20 ducks died at the site; Oo–ike 

pond, 1km distant, also had a cyanobacteria bloom, but no unusual bird 

deaths were reported from that site. Water samples were collected from 

both ponds. Necropsy of one of the affected ducks showed a liver that was 

necrotic and “severely jaundiced...” Preliminary toxicity testing with sonicated cell suspensions using a mouse bioassay resulted in unspecified signs 

of Microcystis toxicity and death within two hours from the Shin–ike pond 

material, whereas that from Oo–ike pond did not produce signs of acute 

toxicity. Quantification of microcystins by HPLC revealed that Shin–ike 

pond lyophilised bloom material contained 318μg/g MC–RR, and 161μg/g 

MC–LR. Oo–ike pond cyanobacteria contained 29μg/g MC–RR and no detectable MC–LR (Matsunaga et al. 1999). While tissues from affected 

birds were not analysed for microcystins, the combination of necropsy, 

bioassay and microcystin quantification, along with differential findings 

between the suspect pond and a nearby “control” site lend strong support 

to the presumptive diagnosis of acute microcystin intoxication in this case. 

Nodularin 

Case study: dog death in South Africa, 1994 (Harding et al. 

1995). 

In March 1994 a bull terrier was admitted to a Cape Town veterinary hospital with a history of lethargy, vomiting and loss of appetite after drinking 

from an urban lake the previous day. The lake is known to be eutrophic 

and the phytoplankton is normally dominated by M. aeruginosa. Antibiotic, corticosteroid, antiemetic and choleretic pharmacotherapy was administered, as well as vitamin B complex and intravenous fluids. Serum 

alanine transaminase was markedly elevated, indicating acute hepatic dysfunction. The dog died on the fifth day after admission; necropsy was not 

conducted, but liver samples were collected and prepared for histopathological examination. Water and scum samples from the lake were col0 I. Stewart et al. 
 621

lected two days after the dog drank from it. Microscopic examination revealed a bloom of 95% Nodularia spumigena, with the remainder being M. 

aeruginosa. Scum material was acutely toxic in a mouse bioassay, with 

liver damage suggestive of cyanobacterial hepatotoxin poisoning. Methanol extracts of bloom material analysed by HPLC with photodiode array 

and UV detection showed a major peak that increased when spiked with 

nodularin standard, and a UV spectrum that matched that of nodularin. Lyophilised cyanobacteria contained 3.5mg/g nodularin; no evidence for the 

presence of microcystins in the bloom material was found. Histology findings suggested toxic liver injury, with hepatocyte degeneration and indications of cholestasis (Harding et al. 1995). Again, while tissues were not 

examined for the presence of cyanotoxins, the combination of clinical 

presentation, diagnostic tools – liver function tests, histopathology, mouse 

bioassay – and investigative chemistry strongly supported the diagnosis of 

nodularin poisoning. 

Cylindrospermopsin 

Case study: cattle deaths in Australia, 2001 (Shaw et al. 2004). 

Two separate poisoning incidents were investigated in Central and Northwest Queensland involving a total of 55 cows. Affected animals were lethargic and recumbent for three or four days ante–mortem. Post–mortem 

findings were typical of cylindrospermopsin intoxication, with pallid livers 

and cholecystomegaly. Histopathology showed hepatocyte degeneration 

and necrosis, nephrosis and multifocal cardiomyopathy. Farm water samples, rumen contents, liver, kidney and muscle were analysed by HPLCtandem mass spectrometry for cylindrospermopsin, which was found in all 

samples except muscle. Water and rumen samples contained cylindrospermopsin concentrations in excess of 1mg/L (Shaw et al. 2004). The principal cylindrospermopsin–producing cyanobacterium in tropical and subtropical Queensland is Cylindrospermopsis raciborskii. Associated stock 

animal deaths and human water supply–related acute and chronic poisonings have long been suspected there (Hayman 1992, Thomas et al. 1998, 

Griffiths and Saker 2003), and livestock industry publications seek to inform farmers, veterinarians and government workers of the risks from this 

cyanotoxin (Berry 2001). 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
6

Anatoxin–a 

Case study: dog deaths in France, 2003 (Gugger et al. 2005). 

Two dogs died in separate incidents in September 2003 shortly after drinking from the shore of a river in the Jura region. Clinical signs were vomiting, hind limb paresis and respiratory failure preceding death. The smaller 

dog (2.5kg) sickened and died shortly after emerging from the water, 

whereas the larger dog (25kg) had a delayed onset of signs and died within 

five hours. Stomach contents, intestinal contents and liver were sampled as 

well as water column and benthic biofilm from the river; stomach contents 

and field samples were examined for phytoplankton identification. An initial screen for three potential cyanotoxins was conducted on biofilm samples: protein phosphatase 2A inhibition assay for microcystins, mouse 

neuroblastoma in vitro assay for saxitoxins, and HPLC with photodiode array for anatoxin–a. No microcystins or saxitoxins were detected, but a 

compound with similar chromatographic characteristics to anatoxin–a was 

seen, so subsequent investigations were directed to that end. A total of 

seven Oscillatorealean cyanobacterial species and genera were identified 

across field and gastric samples; three of these were isolated and one isolate, Phormidium favosum, was found to produce anatoxin–a. This benthic 

species was found in the biofilm covering river sediments, stones and 

macrophytes, as well as from the stomach contents of both dogs – P. favosum being the dominant cyanobacterium found in the smaller dog’s stomach. Identification of anatoxin–a in biofilm, liver and gastro–intestinal contents was confirmed by tandem mass spectrometry; the authors draw 

attention to the necessity for confirmation of identity by fragmentation ion 

spectral assignments to allow definitive identification of anatoxin–a, as the 

amino acid phenylalanine has an identical mass spectrum peak to that of 

anatoxin–a when single ion monitoring is used. This was also the first report of anatoxin–a in French waters, and the first identification of an anatoxin–a–producing Phormidium species. The authors suggest that neurotoxic signs in 37 dogs (with 26 deaths) in 2002 and 2003 in the south of 

France may also have been associated with anatoxin–a intoxication (Gugger et al. 2005). This comprehensive investigation utilised well–equipped 

facilities, use of anatoxin–a and phenylalanine standards, and combined 

expertise in the fields of investigative chemistry, phytoplankton identification and isolation, so it probably represents the current state of the art for 

the diagnosis of anatoxin–a poisoning. 

22 I. Stewart et al. 
 623

Anatoxin–a(s) 

Case study: waterbird deaths in Denmark, 1993 (Henriksen et 

al. 1997, Onodera et al. 1997). 

Cyanobacteria–associated animal deaths have been reported at Lake Knud 

sø since 1981. In 1993, two grebes and a coot that died when a cyanobacterial bloom was evident were collected and frozen. Stomach contents 

were examined microscopically to identify cyanobacteria; Anabaena lemmermannii were found in all three birds. This material was lyophilised for 

further toxin analysis. Four neurotoxic strains of A. lemmermannii were 

isolated and cultured from bloom material collected from the lake. Bloom 

material, cyanobacterial cultures and stomach contents were analysed for 

anticholinesterase activity with a colorimetric assay and for microcystins 

by ELISA. Only low levels of microcystins (ng/kg range) were found in 

bird gastric contents. Neither anatoxin–a nor saxitoxins were detected by 

HPLC. Intraperitoneal injection of bloom material into mice produced 

signs of acute neurotoxicity, including the muscarinic signs of salivation, 

lacrimation and urinary incontinence that typify anatoxin–a(s) intoxication. 

Anticholinesterase activity was significant in bloom samples (2.3mg anatoxin–a(s) equivalents/g); A. lemmermannii isolates and stomach contents 

also showed anticholinesterase activity (29–743μg/g, and 2–90μg/kg body 

weight respectively). Subsequent work using mass spectrometry, nuclear 

magnetic resonance and circular dichroism definitively identified anatoxin–a(s) in bloom material (Henriksen et al. 1997, Onodera et al. 1997). 

Saxitoxins 

Case study: sheep deaths in Australia, 1994 (Negri et al. 1995). 

Thirteen ewes and one ram died next to or within 150m of a farm dam. 

Observed signs were trembling, recumbency and crawling. The ram, which 

was ataxic, was caught by the owner and “immediately died in his arms.” 

Necropsy and histopathology findings were unremarkable. The dam was 

found to contain a bloom of Anabaena circinalis. Mouse bioassay of 

bloom material caused death within 4–11 minutes, with clinical signs of 

staggering, gasping, leaping and respiratory failure. High levels of saxitoxins were found in bloom extracts and intestinal contents of one sheep by 

HPLC with fluorescence detection; principal components were C–toxins 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
6

and gonyautoxins, with low levels of saxitoxin and decarbamoyl saxitoxin. 

Neither anatoxin–a nor microcystins were found using GC/MS and HPLC 

respectively; trace amounts of microcystin–like activity were found with a 

protein phosphatase assay (Negri et al. 1995). Saxitoxin–producing Anabaena circinalis is a particularly problematic cyanobacterium in Australia 

(Humpage et al. 1994). A 1000 km-long riverine bloom in the spring and 

summer of 1991 was associated with significant stock losses; one farmer 

alone reportedly lost over 1,100 sheep during the six–week period of the 

bloom (NSW Blue–Green Algae Task Force 1992, Smith 2000). 

Lesional neurological disease and cyanobacteria? 

The case studies summarised above represent investigations into animal 

deaths associated with the well–characterised cyanotoxins. However, other 

less well–understood cyanotoxins may be capable of killing animals, and 

are being actively researched. Wilde et al. (2005) and Williams et al 

(2007) report on avian vacuolar myelinopathy (AVM), a recently–

described wildlife disease. AVM was reportedly responsible for more than 

100 bald eagle deaths, and “untold numbers” of waterbirds. Clinical signs 

of the disease are loss of coordination on land and in water, and difficulty 

in flying. Necropsy reveals a diffuse vacuolation of myelinated neuronal 

tissue. Epidemiological investigations suggest that a neurotoxin is responsible, with exposure being seasonal, linked to dietary intake by herbivorous waterfowl from AVM–positive waterbodies, and moving up the food 

chain (i.e., from waterfowl prey to eagle predator). Current evidence suggests that AVM is not contagious. A common factor at AVM–positive 

sites – and absent or rare at AVM–negative sites – appears to be an epiphytic cyanobacterium in the order Stigonematales. The authors demonstrate the potential of veterinary epidemiology to advance the understanding of cyanobacteria–related toxicity by use of experimental techniques 

that are not available in the field of human epidemiology. A mallard duck 

sentinel trial was conducted, where 20 farm–raised birds were tagged for 

identification, had wing feathers clipped and were released into an AVM–

suspect pond. The site was regularly monitored, symptomatic birds were 

captured and sacrificed, and at the end of the six–week trial, remaining 

sentinels were captured and sacrificed. Five symptomatic ducks and ten 

birds captured at the end of the trial – these 15 being all birds able to be recaptured from the pond – all showed AVM lesions in brain tissues (Wilde 

et al. 2005). Williams et al (2007) have isolated and cultured the suspect 

cyanobacterium from environmental samples, and have developed PCR as24 I. Stewart et al. 
 625

says to aid detection and identification. Further epidemiological field work 

using suitable control sites would be of great interest. 

“Unusual” animal deaths and cyanobacteria 

The previous discussion has concentrated on cyanotoxin–related deaths in 

common domestic, stock and wild animals. Some other animals reportedly 

poisoned by cyanobacteria are: 

• Flamingos: Cyanobacteria–related mortalities have been reported in 

three flamingo species, both wild and captive (see summary by Codd et 

al (2003)). Lesser Flamingos in Kenyan soda lakes have been the 

subject of research interest, with four microcystin congeners and 

anatoxin–a found in cyanobacterial mats and stomach contents of dead 

birds at Lake Bogoria. Microcystins and anatoxin–a were also detected 

in faecal pellets collected from lake shorelines (Krienitz et al. 2003). 

The same cyanotoxins have been found in feathers taken from poisoned 

flamingos, with a dietary origin most likely (Metcalf et al. 2006). Mass 

die–offs of tens of thousands of birds have been reported in these crater 

lakes, with implications for management and regional and national 

economies, as flamingos are a significant tourist attraction (Krienitz et 

al. 2003, Ndetei and Muhandiki 2005). Isolated strains of Arthrospira 

fusiformis from two crater lakes have been shown to produce both 

microcystin–YR and anatoxin–a, while an A. fusiformis strain from a 

third lake produces anatoxin–a (Ballot et al. 2004, Ballot et al. 2005). 

Similar Lesser Flamingo poisonings have been reported from alkaline 

lakes in Tanzania, with toxic A. fusiformis implicated (Lugomela et al. 

2006). The implications of these findings are significant for several 

reasons, as Arthrospira sp. (also known as Spirulina) are the principal 

food source of Lesser Flamingos, and Spirulina spp. are used as a 

dietary supplement by humans and as a feed additive for livestock. 

There is a significant body of literature that suggests that consumption 

of Spirulina is not harmful (Ciferri 1983, Belay et al. 1993, Hayashi et 

al. 1994, Qureshi et al. 1996, Salazar et al. 1998, Abdulquader et al. 

2000, Al–Batshan et al. 2001), though presumably these studies refer to 

non-toxic strains of Arthrospira used for both commercial mass 

production and from wild harvesting. Investigations to determine the 

relative contribution of A. fusiformis to the production of cyanotoxins in 

Kenyan soda lakes would be of great interest. Some of these lakes are 

periodically dominated by more well–known toxigenic cyanobacteria 

such as Anabaena and Microcystis spp. (Ndetei and Muhandiki 2005), 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
62

so it will be important to estimate the production capacity of 

cyanotoxins by various cyanobacteria in field situations when harmful 

levels of cyanotoxins are present. 

• Insectivorous bats: Staff at a campground in Alberta, Canada, in the 

summer of 1985, counted 500 dead bats and estimated over 1,000 deaths 

on the leeward side of a lake. At least 24 dead mallards were also 

reported. The lake area was covered with a “thick white scum” that had 

a blue–green sheen. Examined animals were covered with a green slime; 

necropsy did not reveal any abnormalities. An alkaloid was extracted 

from the material covering the carcases. This alkaloid was identified by 

GC/MS and found to be anatoxin–a (known at the time as Very Fast 

Death Factor) (Pybus et al. 1986). 

• Rhinoceros: Four white rhinoceroses were introduced to a South 

African game reserve in May, 1979. Two months later, two of them 

were found dead but were unable to be examined. Approximately one 

week later, another rhino was found dead after being seen to be active 

the previous day. Macroscopic and microscopic findings were typical of 

acute hepatotoxicity: hepatomegaly, ascitic fluid, coagulopathy seen in 

various tissues, severe hepatic necrosis and loss of hepatic architecture. 

At the time of death, a severe bloom of M. aeruginosa covered the park 

dam, with a surface scum of 4–12cm (Soll and Williams 1985). 

• Honeybees: In the summer of 1971, “almost total” mortality of bees 

from 84 hives was associated with the insects watering on the leeward 

edge of a lake in New South Wales, Australia. That area of the lake was 

affected by a windborne scum of A. circinalis; an apiary on the 

windward shore was unaffected (May and McBarron 1973). 

Exposure routes, avoidance behaviour 

Exposure to cyanotoxins in the field is presumably either through contaminated drinking water or by direct consumption of benthic cyanobacteria. Codd et al (2005) also note suggestions that cyanotoxins may move 

along the food chain to poison wild animals. This would seem to be a plausible interpretation: there is a significant section of the literature devoted to 

experimental and observational studies of cyanotoxin bioaccumulation and 

trophic transfer. Much of the literature is concerned with potential human 

exposure to cyanotoxins through consumption of molluscs and fish; shortterm (days, weeks) accumulation of hazardous levels of cyanotoxins in 

aquatic prey is certainly feasible, and predator animals may be more at risk 

6 I. Stewart et al. 
 627

than humans in some circumstances, since they are more likely to consume 

the viscera in which cyanotoxins are found in highest concentrations. Several bioaccumulation studies are inconclusive; for some positive examples 

see: (Negri and Jones 1995, Saker and Eaglesham 1999, Magalhães et al 

2001, Sipiä et al 2002, Saker et al 2004, Sipiä et al 2004, Smith and Haney 

2006). 

Experimental work has shown that the inhalation route may be an efficient 

method for microcystin–LR to access the circulation (Creasia 1990, 

Fitzgeorge 1994, Ito 2001), but there is no evidence that cyanotoxins can 

be effectively aerosolised to toxic concentrations under field conditions. 

The topic of inhalational exposure to cyanotoxins is clearly under–

researched at present. 

Codd et al (1992) outlined the premise that exposure to toxic cyanobacteria may not always be coincidental; dogs may actively seek out and consume benthic cyanobacteria. Some descriptions in the report of Hamill 

(2001) also suggest that dogs may actively consume toxic cyanobacteria. 

The work of Gugger et al (2005) also appears to support this concept: 

while descriptions from the field were that two dogs died “soon after 

drinking water from the shoreline of the...river...” analysis of phytoplankton in the dogs’ stomachs revealed the presence of biofilm–associated 

cyanobacteria that were not seen in water column samples. This thick 

biofilm reportedly covered sediment, stones and macrophytes at the water’s edge (Gugger et al. 2005); it is at least conceivable that those animals 

were also actively consuming toxic cyanobacteria for their final meal. 

As for planktonic cyanobacteria, there are suggestions that wild and 

domestic animals will avoid drinking from cyanobacterial scums if less–

affected water is accessible. Falconer (2005 p.80) notes that detailed investigations of cyanobacteria–related stock animal deaths often reveal that 

cleaner water was unavailable because of fence lines, thus forcing the animals to consume toxic water. Other workers have reported avoidance behaviour in cattle (Codd 1983) and flamingos (Ndetei and Muhandiki 

2005), but Carbis et al (1994) report that sheep did not discriminate between hepatotoxic cyanobacteria–contaminated water and a readily available alternate supply. Lopez Rodas and Costas (1999) report observing ungulates, birds, wasps and unspecified wildlife failing to demonstrate 

avoidance behaviour, consuming concentrated M. aeruginosa scum in 

Spanish reservoirs. Their subsequent experiments showed that laboratory 

mice demonstrated an ultimately fatal preference for dense cultures of microcystin–producing M. aeruginosa over tap water, and they did not discriminate between toxic and non–toxic strains of M. aeruginosa in their 

drinking water. Steyn (1943) noted that pregnant animals and dairy cows 

displayed a preference for consuming Microcystis scums, suggesting that a 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
628

relative nutritional deficiency may explain higher mortalities than seen in 

dry cows. 

Treatment of affected animals; research needs

As no complete pharmacological antagonists against cyanotoxins are 

available, treatment of affected animals is largely supportive. Purgatives 

and enemas may be helpful; unguents and restriction to shaded areas 

should be considered for animals suffering secondary photosensitization 

(Steyn 1943). Other supportive therapies include emesis, activated charcoal and bathing to remove bloom material from the fur (Corkill et al. 

1989, Roder 2004). Blood transfusion and correction of electrolyte imbalance has been recommended (Beasley et al. 1989a). Aggressive intervention with fluid replacement and steroids has been suggested for cases of 

cyanobacterial hepatotoxin poisoning (Roder 2004). While such an approach was unsuccessful in the case (discussed above) of the bull terrier 

presumed to have died from nodularin intoxication (Harding et al. 1995), 

there is clearly a need for controlled experiments to evaluate interventional 

therapies. Pre–treatment with pharmacologic doses of hydrocortisone prevented acute and delayed MC–LR–related mortality in mice (Adams et al. 

1985), and dexamethasone and indomethacin pre–treatment blocked renal 

toxicity caused by MC–LR (Nobre et al. 2001). Pre–treatment with steroids is obviously not a practical therapeutic intervention, but these findings 

suggest that there is much more to be learned about the immunotoxicology 

of the cyanobacterial hepatotoxins. 

Artificial ventilation has been suggested in cases of cyanobacterial neurotoxin poisoning (Beasley et al. 1989a, Beasley et al. 1989b, Carmichael 

and Falconer 1993, Roder 2004). While the practical application of this 

technique in the field would present significant challenges, experimental 

work to evaluate the benefits of intermittent positive pressure ventilation 

and other intensive therapy may have implications for the field of human 

medical care as well as for economically valuable equine and livestock 

animals. Work conducted in the 1970s on calves and rodents dosed with 

anatoxin–a–producing cyanobacteria suggested that artificial ventilation is 

unlikely to be a practical intervention, with one calf failing to achieve effective spontaneous respiration after being ventilated for 30 hours, and rats 

similarly afflicted after maintenance ventilation of up to eight hours (Carmichael et al. 1975, Carmichael et al. 1977). However, anatoxin–a doses 

producing up to 95% neuromuscular blockade in rats were reportedly reversible with respiratory support (Valentine et al. 1991). Artificial ventila-

 I. Stewart et al. 
 629

tion was conducted on three rats during experimental administration of 

anatoxin–a(s); they survived a greater than 4–fold lethal dose in the short 

term (less than one hour), but the study was not designed to follow through 

to recovery (Cook et al. 1990). Interventional strategies to treat saxitoxin 

poisoning using antitoxin or the potassium–channel blocker 4–

aminopyridine and artificial ventilation have shown promise, though the 

toxicodynamics of saxitoxin are complex and the combined neurological, 

cardiovascular and respiratory effects are incompletely understood (Chang 

et al. 1993, Benton et al. 1994, Chang et al. 1996, Chang et al. 1997, Benton et al. 1998). 

Management of seizures, presumably anticonvulsant pharmacotherapy, 

has been suggested in cases of cyanobacterial neurotoxin poisoning (Roder 

2004), though this may be a moot point if, as suggested at least for anatoxin–a, seizures result from hypoxia–related cerebral ischaemia (Carmichael 1994). Cyanobacterial neurotoxin–related seizures are not well described in the literature, mostly being referred to as “convulsions”, though 

there are references to clonic spasms (McLeod and Bondar 1952), clonic 

seizures (Cook et al. 1989, Cook et al. 1998, Carmichael 2001), tonic 

spasm (Firkins 1953) and tonic seizures (Beasley et al. 1989a, Beasley et 

al. 1989b). The electrophysiology of these events has not been investigated. Opisthotonus is often described (Carmichael et al. 1975, Gorham 

and Carmichael 1988, Cook et al. 1989, Carmichael 2001, Codd et al. 

2003); this increase in tone of the musculature of the neck and shoulders 

has some similarity to the clinical manifestation of a tonic seizure, though 

again the priority from a management perspective would appear to be restoration of oxygen to the tissues. Anticonvulsants have also been administered for management of seizures in cases of cyanobacterial hepatotoxin 

poisoning, but with little apparent benefit (Corkill et al. 1989). 

Further empirical studies are warranted to assess various emergency interventions, including pharmacotherapies, for cases of cyanotoxin poisoning. However, these are potent, rapidly acting toxins, so prevention will 

likely remain the most effective intervention for the foreseeable future. In 

the short term this involves restricting access to cyanotoxin–affected drinking water, with longer–term strategies of nutrient reduction to mitigate 

blooms. Dissemination of information to farmers and the livestock industry is always important; beyond the academic research literature there are 

some industry and government partnerships that provide helpful resources, 

e.g. Australia’s Animal Health Surveillance Report (see for example Berry 

2001, Elliott 2001), and the Animal Health Expositor from Canada (now 

Animal Health Perspectives) (Yong 2000a, Yong 2000b). Comprehensive 

economic analyses of the costs of cyanotoxin–related livestock and wild 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds
63

animal poisonings to the agricultural and tourist industries would be valuable. 

Concluding remarks 

Cyanotoxins in the environment continue to be hazardous to livestock and 

wild animals throughout the world. While much is known about the most 

potent, acutely toxic neurotoxins and hepatotoxins, there is still more to 

learn about the toxicokinetics and toxicodynamics of even the well–

characterised cyanotoxins. Cyanobacteria are rich sources of biologically 

active compounds, and it is likely that some yet–to–be–described cyanobacterial products will be found to be harmful. Current investigations into 

the subacute disease avian vacuolar myelinopathy hint at this possibility. 

While controlled dosing with purified cyanotoxins under laboratory conditions has been an essential endeavour that allows these materials to be 

characterised and understood, exposures in the field may be much more 

complex. Subacute or chronic exposures, particularly to hepatotoxic 

cyanobacteria, may result in clinical presentations characterised by concomitant degenerative and regenerative changes. Expert veterinary clinicians and pathologists, as well as specialist investigative chemistry laboratory services, are invaluable resources for the diagnosis and management 

of these complex poisonings. 

Acknowledgements 

Thanks to Wasa Wickramasinghe for helpful discussion. This work was 

supported by the Cooperative Research Centre for Water Quality and 

Treatment. 

The National Research Centre for Environmental Toxicology is co–

funded by Queensland Health, The University of Queensland, Griffith 

University and Queensland University of Technology. 

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Yong C (2000a) Cyanobacteria (blue-green algae) poisoning. Animal Health Expositor 2(3):2 http://www.usask.ca/pds/Information/Sept%20%2700.pdf 

Yong C (2000b) Blue–green algae poisoning in two dogs. Animal Health Expositor 2(3):3 http://www.usask.ca/pds/Information/Sept%20%2700.pdf 

Chapter 28: Cyanobacterial Poisoning in Livestock, Wild Mammals and Birds