Roo Gully Report sent with Missy's body to Murdoch University in Perth - 6th August 2004

History:
19th March 2004
Arrived at Roo Gully after mother killed in road accident near Collie.
Joey had no apparent injuries and appeared to be in good health.
Usual however to note she did not have any ticks, but she had spent 25 hours at Collie Veterinary Hospital
during which time they could have vacated.

Measurements on Arrival:
Weight - 1.275 kilograms
Tail measurement - 425 mms
Foot measurement - 160 mms

Medical Problems:
Appeared to be in good health throughout her time in care, with no episodes of diarrhoea
17th May it was noticed her urine was slightly darker and redder in colour -
milk formula was changed to a weaker brand and solution - problem cleared up with no other treatment

2nd August
Came into house during the evening and looked lethargic - still feeding
We noticed she had lost what appeared to be a massive amount of weight in a very short period -
maybe as much as 500 grams in 36 hours
Wormed with Virbamec - 0.3ml (Pour On) - Active constituent - Abgmectin 5mg/ml
Still feeding as usual
Stayed inside the house during the night

3rd August
Rapid decline overnight - lethargic, weak, difficulty standing
Taken to Collie Veterinary Hospital - initial examination diagnosis severe bacterial infection
Temperature (Rectal) - 36C - hypothermic - Placed in humidicrib
250mls of 5% Glucose - IV plus multivitamins
0.5ml + further 0.25ml Dexamethazone - IM
0.5ml Baytril (50mg/ml Enrofloxacin) - IM
Returned to Roo Gully:
2nd IV drip - 1 litre Hartmanns Solution + 50mls 50% Glucose to run over 2 days
Baytril (50mg/ml Enrofloxacin) to continue - 0.5ml IM for further 3 days

Remained lethargic, but showed an interest in eating native grasses and plants

Urine sample:
PH - 6
Leucocytes - Moderate
Protein - 1.0
No blood

4th August 2004
Lethargic at times - but with episodes of alertness during which time she would stand and eat
08.15: Drank 15mls - Formula One + half teaspoon Glucose powder
09.15: Stood and ate kangaroo nuts, grevillea, lucerne
Urine sample:
Glucose - trace
PH6.5
Protein - 1.0
Leucocytes - Moderate
09.30: 0.5ml Baytril (50mg/ml Enrofloxacin) - IM
12.00: Drank 14mls Wombaroo 0.7 with added Impact + Glucose powder
Urine sample:
PH - 6.0
Protein - 0.3
Leucocytes - Moderate to Small

During the afternoon ate very well - native grasses and plants - grevillea, lucerne, wattle
14.15: Urine sample:
pH 6.5
Protein - 0.3
Leucocytes - Moderate to Small

18.00: Appeared to be suffering from severe gut pain, 'mini' convulsions
0.3ml Pamlin (Diazepam 5mg/ml) - IM
0.3ml Rimadyl (Carprofen 50mg/ml) - IM
18.15: Was experiencing good pain relief and steady sedation - comfortable
Good heart rate and respiration - soft bowel sounds
21.15: Standing up and eating well
21.30: Urine sample:
Glucose - 15
PH 6.5
Protein - 0.3
Leucocytes - Moderate to Small

5th August 2004
3.00: Awake, standing and eating well - passing urine and good faeces
6.45: Grinding teeth, looked uncomfortable, progressed to convulsions
07.00: 0.3ml - Pamlin (Diazepam 5mg/ml) - IM
08.30: Convulsing
0.3ml Pamlin (Diazepam 5mg/ml) - IM
0.3ml Rimadyl (Carprofen 50mg/ml - IM
09.15: Still convulsing - 1ml Pamlin (Diazepam 5mg/ml) - IM
10.00: Missy died

Blood samples taken from heart soon after death

Please note:
Other Western Brush wallaby, 2 years old, at Roo Gully lives in the same area as Missy did,
and so far appears to be in good health.

2 other Western Brush wallabies have been cared for at Roo Gully. Both females.
The first one died in similar circumstances to Missy. She was apparently in previous good health, apart from suffering head injuries from road accident, and suddenly began convulsing and died within one hour.
The other wallaby reached maturity, was in excellent health and was killed by a fox.

Diet and Weight Data:

19th March 2004
Weight - 1.275 Kilograms
Fed Wombaroo 0.7 - 20mls x 5 per day

20th March 2004
Weight - 1.308 Kilograms - 33 gram gain - probably due to fluid replacement

21st March 2004
Weight - 1.345 Kilograms - 16 gram gain

25th March 2004
Weight - 1.377 Kilograms - 69 gram gain in 5 days (14 grams per day)

3rd April 2004
Weight - 1.584 Kilograms - 207 gram gain in 9 days (23 grams per day)
Showing an interest and eating some solids and natural food
Kangaroo nuts, oats, grevillea, grass and also eats dirt

8th April 2004
Weight - 1.751 Kilograms - 167 gram gain in 5 days (approx. 33.5 grams per day)

15th April 2004
Weight - 1.842 Kilograms - 91 gram gain in 7 days (13 grams per day)
Reduced weight gain thought because she was now more active. Spending less time in her pouch and being introduced to being outside with other wallaby, Winnie
Missy also not sleeping for long periods at night

24th April 2004
Weight - 2.080 Kilograms - 248 gram gain in 9 days (23 grams per day)
Now spending more time outside with Winnie, grazing and browsing, which could account for better weight gain.

1st May 2004
Weight - 2.235 Kilograms - 155 gram gain in 7 days (22 grams per day)
Now down to 2 feeds of Wombaroo 0.7 per day and outside at night

10th May 2004
Weight - 2.483 Kilograms - 148 gram gain in 10 days (18 grams per day)
Refusing evening bottle, so now only on one bottle a day of Wombaroo 0.7

17th May 2004
Weight - 2.653 Kilograms - 170 gram gain in 7 days (24 grams per day)
Noticed that her urine was slightly darker and redder in colour.
Milk formula changed to Formula One - the reason being we have noticed before that joeys being fed Wombaroo 0.7 that are approaching weaning are more prone to urinary infections. We suspect the milk might be too strong for them at this stage
Formula One offered at 40mls x 2 per day.
Now outside and weaned slowly to no bottles

2nd August 2004
Weight - 2.835 Kilograms - lethargic - first sign of illness - and had lost weight in previous 36 hours

History:
The wallaby was presented at Collie Vet Hospital on 3/8/2004.
Very weak, laterally recumbent, pale mm., shallow breathing, cold Temp. 35.8C.
Treatment plan was symptomatic:
250ml 5% glucose IV (prewarmed/over 2 hours) 0.5ml Multivitamins IV
0.25ml 2omg/ml Dexamethosone IV 0.50ml Dexamethosane IM
0.50ml Baytril IM (50mg/ml).
Placed in humidicrib at 28oC. Marked improvement.
Urinalysis: Leukocytes 75/ul; protein 100mg/dl - combin strips.
1l Hartmans IV slow.
Temp 36.5C. All vital signs improved, more alert. Sent home on fluids to be cared for at Roo Gully.
After initial improvement the Wallaby died on 5/8/04. Vet not present at time of death. No diagnosis was made. We have had several wallabies and joeys of this age group die under similar circumstances without definitive diagnosis. We have been able to make one diagnosis of calcinosis circumscripta in our older wallaby which had had a similar history when younger but survived.

MISSY
POST MORTEM REPORT
MURDOCH UNIVERSITY, PERTH
Pathologist - Dr. Phillip Nichols

Submission:
Status: Post natural death.
Post mortem interval:
Post mortem decomposition: minimal
Identifying features:

Visible lesions:
Significant External Findings
Severely emaciated carcase.

Significant Internal Findings
Saccular stomach and intestines full of ingesta.
Colon contained faecal pellets.

Gross Summary:
No visible lesions were seen on gross examination, although the poor body condition suggests a chronic condition was present also.

Ancillary Tests:
Microbiology - CP3145 / 04.
Aerobic culture from the lung yielded a moderate growth of a weakly alpha-haemolytic Streptococcus species.
Aerobic culture from the liver yielded a scanty mixed growth including a weakly alpha-haemolytic Streptococcus species.
Selective culture for salmonella from the caecum contents proved negative.

Antibiotic sensitivity
The Streptococcus isolated above was sensitive to penicillin, cephalexin, amoxy/clav, erythromycin, Sulph/trim and tetracycline, with intermediate sensitivity to lincomycin.

Parasitology - CP3145 / 04
No parasitic organisms detected on Malachite Green Stain, Zinc flotation or Faecalizer.

HAEMATOLOGY COMMENTS: leukopenia, neutropenia, mild anaemia

Biochemistry
LABORATORY SAMPLE/SITE & TEST REQUESTED:
EDTA: cbc
Serum: panel
Faeces: parasites
Liver, lung: culture
Caecum: salmonella

BIOCHEMISTRY COMMENTS:
CommentsNo bilirubin result as sample was haemolysed
Was the sample taken post mortem?

Histopathological findings:
H04-0510A. Lung x 2, liver. Pleura normal. Alveolar capillaries show diffuse moderate acute congestion. Alveolar airspaces appear clear, bronchioles and pulmonary vessels appear normal. Lungs show mild to moderate sinusoidal congestion and some post-mortem dissociation of hepatocytes, capsule normal and portal triads normal.
H04-0510B. Heart x 2, kidney, spleen. Endocardium, epicardium, myocardium and Purkinje fibres normal. Spleen appears mildly contracted and with prominent periarteriolar lymphoid sheaths (as expected in a young animal). Kidney has multifocal basophilic and irregularly shaped lameliar concretions in tubules of the cortex and interstitium (calcification), and occasionally in vessel walls. Tubules and glomeruli otherwise normal.
H04-0510C. Adrenal, lymph node, intestine x5. Sections of gastrointestinal tract show mucosal autolysis, otherwise normal. Adrenal, lymph node and pancreas appear normal.
H04-0510D. Central nervous system x3. Medulla oblongata, pons and cerebellum, of questionable significance, but no other changes are seen.
H04-0510E. Cerebrum. A section of cerebrum appears normal.
H04-0510F. Tongue x2. Two sections of tongue appear normal.

Final diagnosis:
Inconclusive

Final Comment:
The investigations detailed above failed to confirm a significant underlying disease. Despite the overall thin condition, there was no evidence of chronic parasitism, or chronic bacterial or viral infections. Specifically, there was no histological evidence of macropod herpes virus, which causes a multifocal necrotising hepatitis and a pneumonia. A streptococcus was isolated from both liver and lung (sensitivity detailed above). Whilst this could reflect an acute systemic bacterial infection, no histological evidence of acute or chronic inflammations was seen, although this may of course reflect an even distribution of lesions within the tissues. There was some multifocal calcification in the kidney, but this is not considered significant in relation to the death. The serum biochemistry shows very high CK levels and other anomalies. Given the species and the high CK levels (>70,000), a capture-type myopathy must be considered as a possibility here. Although some capture myopathies are associated with gross lesions of heart and skeletal muscle, some capture myopathy shock syndromes show very little grossly except perhaps pulmonary congestion and oedema and a few other rather non-specific findings. Additionally, the affected muscle groups can be very focal, and so unless every muscle group is sampled, the findings can be minimal. Even histologically, lesions can prove few and far between. Although conclusive proof is hard to demonstrate, in this case the serum biochemistry suggests that a peracute myopathy shock syndrome is a possibility. This should be interpreted alongside a consideration of any recent handling, restraint, or possible chasing be children or dogs.