Download ELUSIVE BACTERIUM

Kitten Season Is Upon Us
and sadly some kittens will not survive the first days and weeks of life
A likely culprit – Streptococcus G
One of the greatest pleasures of cat breeding is celebrating the safe arrival of a litter
of healthy kittens. Watching an unfussed queen have an easy labour, deliver her
kittens competently and happily, and go on to rear a litter of bright-eyed, bouncy,
happy, friendly little cats is the “best it can get” experience. Unfortunately it is not
always like that.
UNEXPLAINED KITTEN DEATHS
Sometimes things go wrong. Kittens get sick, sometimes very sick, and deteriorate
rapidly. Onset of illness can be hours, days or a few weeks after birth, and
progression of the infection is characteristically rapid – well in the morning, dead by
nightfall or the next day or two. You rush to the vet, come home with antibiotics,
kitten milk replacer, subcutaneous fluids, and watch as the tiny kittens struggle to
live.
Standard URTI treatments are usually prescribed, but they aren’t very
successful.
Some kittens do recover if they are treated early in the course of the infection, but
there are litters where, despite best efforts, some kittens succumb to intractable
upper respiratory disease, losing weight and losing strength, and within hours or a few
days, dying. Sometimes none survive. Does this scenario sound familiar? It’s a
mystery bug that is rapid and lethal for kittens. This is the profile of Streptococcus
G infection.
STREP G
Strep G is a bacterium that can live on the queen’s vulva and vagina, causing her no
problem. It is introduced to the kitten’s respiratory tract during birth, and rapidly
becomes rampant. A bacterial weed – growing like mad in the wrong place.
The surviving female kittens are almost certainly carriers from this early age, as the
queen already is. Strep G cocci which find their way into the female kittens’ vaginas
are ready for the next generation of kittens to be infected. Unless Strep G is
eradicated, the pattern will likely reoccur in infected females in subsequent
generations.
HOW INFECTION HAPPENS
Cats pass Strep G around because of the friendly mutual grooming habits, licking the
genital areas of friends and themselves. Queens grooming their kittens infect the
kittens. Infected “aunties” can do the same thing.
HOW CAN I TELL IF MY CATS MIGHT HAVE STREP G?
Here’s how to go about it. Go back through the breeding records of all of your
breeding stock, and list the following. Yes, write the information down; you can use it
in discussions with your vet later. Seeing the information written down makes it
easier to see the overall picture.
The pattern in your cattery over time is the
evidence you need to make your case for treating your cats.
For every queen, note the following:
1. Is she a survivor of a litter where one or more kittens died of respiratory
illness?
2. Has she had aborted or absorbed litters?
3. Has she delivered any dead kittens early or full term?
4. Has she, at full term, been in labour that was half-hearted, sporadic, and
eventually needed veterinary intervention? Has she evidenced uterine inertia?
5. Has she had kittens where one or more became very ill, and even died in the
period from 24 hours to 2 months after delivery?
6. Has that pattern repeated in subsequent litters?
7. With different studs?
8. What treatment was prescribed?
9. How well did it work?
10. What was the survival rate, and how long did the kittens live?
11. Did you have any tests done and what were the findings?
12. Any autopsies? What were the findings?
13. Have any of her daughters been bred, and what are their relevant histories?
Create this list for each of them.
14. What about her mother? Create this list for her too.
Look for patterns, clusters of these events occurring over time and involving some or
all of your queens. Include females you may have sold for breeding. The pattern is
the clue that there is a persisting underlying problem that has not been correctly
treated, probably because it has never been accurately diagnosed.
If your own research reveals some or all of these 14 issues in your own cattery, take
one or more of your affected queens to your vet for a vaginal swab to test for Strep G.
SPECIAL TEST FOR STREP G available at Gribbles Veterinary Pathology Laboratory
(some path labs don’t test for Strep G). Tell your vet to order GVPL to (1) determine
if Strep G is present in the cat’s vagina, and (2) to culture and do drug sensitivities.
Your vet will have the details for GVPL.
ERADICATION
Clindamycin kills Strep G. Treat with Clindamycin (Antirobe) daily for 21 days. This is
safe for pregnant cats. Treat all your cats as described above.
Routinely weigh kittens daily, and if there is no weight gain, or a loss, and the queen
has milk, start treatment immediately. The sooner treatment is begun the better the
outcome. Don’t wait until tomorrow; it may be too late, and the kitten may already
be too sick to recover.
Control requires treating every cat in your cattery, male, female, entire, desexed, with
clindamycin for 21 days. If you house your cats in separate colonies, treat every
member of each colony at the same time, and do not allow any intermixing between
members of treated and untreated colonies, or you will reinfect the treated cats.
Read below how Strep G was identified as the cause of unexplained kitten deaths,
and what medical interventions and cattery practices worked to manage this
distressing problem.
Source: Appendix 11, Breeding Cats: A Practical Guide (rev). Truda M Straede.
Self published, 1997.
Streptococcus G
THAT ELUSIVE BACTERIUM
A Study in the Pursuit of an Australia Wide Feline Health
Problem in the Early 1990’s
This article combines elements from articles and letters published in the RAS Cat
Control Journal from August 1993 to February 1995. The problem described in the
very first article ‘It’s easy to see the Pattern - In Retrospect’, struck a chord with
readers throughout Australia, and contacts were made with me from as far away as
Darwin - and New Zealand. At the time of publication of the second part of the first
edition of Breeding Cats…. a practical guide, I still had occasional requests from
breeders to help them to solve similar problems. Some of those who were helped in
the past requested that the salient articles be included as an appendix in that second
volume. After a break of 10 years or so, where Streptococcus G appeared to have
somewhat faded into the background, there was a new wave of problems of a similar
nature reported in Australia, but in the meantime there had been a ripple affect
worldwide, with similar problems in far flung places being treated as recommended
here. Emails1 from all over the world have come to me asking for help, which is why I
consider that it is worthwhile reprinting this saga as an example of what we as
breeders can do with co-operation amongst ourselves, friendly vets and
pathologists….
Big pharmaceutical companies and universities have
their own
research agendas, not always interested in responding to the concerns of breeders,
but we should not ‘lie down and take it’, but attempt to move the agenda onto our
concerns.
In August 1993 I first reported on the RASCC Journal a rash of problems, which had
been occurring amongst my cats for the previous 12 months. As I had by this stage a
wholly Leukaemia free cattery, with all breeding stock Leucogen vaccinated, I was
becoming very dispirited with a cattery wide rash of late abortions, and fading kittens.
My cattery was free of Leukaemia so why was I having these problems, so
indicative of a Leukaemia outbreak?
In addition to the kittens which were fading from a few days old, the longer lasting
ones on autopsy showed massive involvement of the lungs. They were totally
unresponsive to Chloramphenicol, Amoxil, Clavulox, Tylan and Penstrep, where could
this apparent flu infection have come from? Several of these same queens had had
healthy normal kittens in the past.
In January 1993 I was losing a litter of 7 one by one - the first died within 48 hours
after a sudden weight loss, this is how I described what happened:
10-12-92 Quassia has seven beautiful robust kittens to Jolyf. Quassia herself
initially a bit off colour - Penstrep shots, yoghurt for her and all her kittens, all settled
down by 15 Dec. Suddenly on 23-12 one of the two boys lost weight, supplemented
this one, and others with yoghurt/Energel cream and iron supplement. 10-1-93 this
male suddenly took a nose dive in weight and other male also suddenly lost weight.
Autopsy first male - some lung congestion - all kittens onto Clavulox and Mucodine.
12-1 all starting to go down hill rapidly - assessed chances as: one definitely dying,
two with only days to go, one sickening, and one normal weight. Why not try
Antirobe? There was nothing to lose. (Antirobe was very new at this time).Within an
hour the dying one was dead, the two really ill ones were running around looking
bright eyed - though it took me a lot of careful feeding and it wasn’t till the 16th that
these two started to eat by themselves, the litter never looked back - but please note,
I did not treat Mum.
This was only the beginning - I had further problems with later litters from queens
where only the kittens were treated, and even when I also treated the queens I still
had residual problems. I came to the conclusion that the causative/ bacterial agent/s
can be carried in a latent state. While I managed to destroy the internal
manifestation so that kittens were carried to term, it looked very much as though it
lodged in the respiratory passages, and could be shed over the kittens by the mother.
As kittens fell prey to the infection at about the same time as they would if it were
viral (ie about 5 weeks on, when maternally derived antibodies are wearing off), it
was hardly surprising that it was lumped with ’cat flu’ in the mind of vet and breeder
alike.
Gathering up my personal experiences and those relayed to me by many other
breeders, this is how I summed up my thoughts on this problem:
? MICRO-AEROPHILIC BACTERIA in CATS Truda M Straede 15-6-94
What did we know?
1 An Antirobe (Clindamycin) sensitive organism was involved with cases of early
abortion, premature birth, low birth weight weak kittens, reluctance to go into labour,
perinatal deaths and some concurrent congenital defects.
2 An Antirobe sensitive organism was involved with some kitten deaths, which may
start as soon as a few days old, and may continue sporadically till all the kittens die,
as old as 8-9 weeks, or until a couple of weeks after the kittens are removed from
their mothers. Kittens typically looked normal, gained weight normally, till a sudden
weight drop occurred over night, after which they withered away in 4-5 days,
apparently unresponsive to any antibiotics, unless Antirobe was used. These kittens
usually, but not always appeared to be dying from an acute upper respiratory tract
infection, and on autopsy showed lung changes which confirmed this. Even kittens
which showed no external signs, eg sneezing, stuffy noses and inflamed and stuck up
eyes, on autopsy showed extreme changes consonant with pneumonia. Mother cats
often also looked a bit off colour when this happened to their kittens, with depressed
appetites and lack of interest in their kittens.(eg my queens Zouiidi, Quassia)
3 A queen treated with Antirobe, quite aggressively ie 14 day course, at the time of an
episode such as 2, may have a perfectly normal litter next mating. (eg my queen
Kit'n'Caboodle was treated with litter number 3, number 4,5,6 all OK.)
4 A queen (Quassi) not treated with Antirobe at the same time as her kittens were
(the 4 week old kittens had responded like magic when they had been dying one by
one), had a litter one week premature next time, all of which died (one was also
deformed) at birth. After this she was treated with Antirobe. Her next litter was full
term, but had some problems at about 4 weeks old, both they and Mum were treated
with Antirobe. Her next litter was without problems throughout, in these last three
litters, the sire was the same.
5 A queen treated with Antirobe both from the start of a call and throughout
mating, (at least 10 days) and from week 5-6 of the pregnancy has an
excellent chance of having a perfectly healthy litter, which grows very well
and is remarkably trouble free. This treatment is equally successful whether
the queen has been only in contact with queens affected in the past, or has
herself lost a litter in one of the ways described above.
6 Young queens with their first litter may have some of the problems outlined in 1, if
their mother was affected, whether she, or they were treated or untreated at the time
of the first occurrence of symptoms in either. These young queens respond to
treatment 0-1, 5-6 weeks of their next pregnancy, rearing strapping healthy babies.
7 A queen (Bisquit) who lost her first litter apparently because she failed to go into
labour in time (only 2 kittens) appeared to be healthy. She became pregnant again,
but in the last 10 days of pregnancy succumbed to an upper respiratory bug, for
which sensitivity testing indicated a penicillin group treatment. She failed to respond
adequately - so was treated with Antirobe, and was definitely on the mend within 24
hours. Quite unaided she produced an on time litter of one very large, healthy kitten,
which thrived.
8 An only survivor kitten from a case such as 2, grew into a perfectly healthy brood
queen (Bella). Called, mated, carried litter - till almost (62 days) term. Two
apparently fat healthy kittens, and one dead at birth because labour was also
protracted as well as early. Kittens lived for 8-10 days - apparently died of acute
pneumonia. I then realised that mother was only survivor of the first litter of a queen
whose only other litter was treated aggressively with Antirobe. Bella had never been
treated with Antirobe till this kitten loss.
HYPOTHESIS
By drawing a parallel with what Kim Kendall had told me about Contagious Equine
Metritis,1 caused by a micro-aerophilic bacterium, carried on the mare's vulva, which
causes no symptoms or disease in the mare, but when it is enabled to pass into the
uterus during mating, causes early abortions, premature births and neonatal losses,
(it is thought to be transmitted by the stallion from mare to mare) I surmised that our
losses could be caused the same way by a similar type of organism.
Firstly, though many samples were sent off to pathology labs by my vet (Karen
Hedberg) who was quite concerned about the apparent epidemic amongst many
breeders, the results had been either no growth, or a range of other organisms,
including most frequently, Pasteurella multicida which were unlikely to be the main
cause. Such a result would not be surprising, if the causal agent was indeed a microaerophilic bacterium, which would elude all the routine tests, because of its very
specialised environmental requirements.
Secondly, causes other than bacterial were fairly clearly ruled out because of the very
dramatic response to one specific antibiotic, Clindamycin, used generally for anaerobic
bacteria, including some pretty nasty ones! Some concern was felt, not only by me,
that this antibiotic, so important in treating very refractory and serious conditions,
should not be indiscriminately used - a good reason why actually tracking down the
cause, studying it specifically, developing a lab test for queens, and working out an
effective treatment that doesn't encourage the growth of drug resistance is very
important.
Thirdly, queens appeared to be able, like mares, to carry this organism with no
adverse effect to themselves - the trouble only started with mating. This once again
suggested the inside/outside type location, such as the vulva as the preferred site for
the bug, allowing ready entry through the cervix at mating.
Fourthly, unlike mares, cats behave in such a way that transmission horizontally, from
queen to queen is very probable (I have no evidence implicating studs) - queens live
in colonies, and it is the height of feline good manners for them to lick each other's
bums - and then their own.
Fifthly, the constant grooming of neonates by their mothers, who are also assiduously
grooming themselves, particularly, after birth, their rear ends, gives abundant
opportunities for vertical transmission, the bug to be liberally smeared all over kitten
bums and mouths, for it to enter the lungs, giving a set of symptoms which are
absent in the mare/foal interface because of differences in behaviour, but also
creating a new generation of carrier queens.
1
B.Rogerson, Contagious Equine Metritis Bacteriology Vic IInst of Animal Science, Dept of Ag Equine Veterinary Science
8(1), 1988
SOME NIFTY BUG As an ecologist I was full of admiration for its exploitation of an
obscure niche; one where it was so ‘safe’!!
By the time that I had come to this conclusion, I had begun to have confirmation from
breeders all around Australia and as far away as New Zealand that I was not alone.
They came as timid calls, guarded calls, anonymous calls and letters for the RASCC
Journal where the name was to be withheld. I invoked the wrath of one vet, who
wrote a letter very critical of my whole hypothesis, but equally, I had many calls from
vets who had clients who wanted to use the treatment we had worked out. I talked to
them, I passed them on to my vet (Karen Hedberg BVSc), they were, if not convinced,
at least prepared to try the treatment regime.
One Australian Mist breeder, who had also suffered the same kind of problems, was,
by chance, an outstanding Microbiologist. She prepared an answer for a critical vet,
which was printed in the RASCC Journal in May 1994. Her letter is reprinted here in
full as it provides not only a measured answer to the specific criticisms made by the
vet, but also presents a well reasoned view of the balance between vet, hobbyist and
professional, and is of interest in its own right.
The Editor
As an experienced microbiologist (virology and epidemiology), cat breeder and
Victorian reader of the RASCC Journal, I have read with interest the series of articles
(Aug and Nov 93) and arising correspondence (Feb 94) concerning diagnosis and
treatment of infectious diseases in cats and litters of kittens. In particular I would like
to draw attention to comments made by Nicholas Jonsson (Feb 94). He quite correctly
states that Pasteurella multocida may be a normal inhabitant (flora) of the mouth and
respiratory tract of most normal cats.
BUT WHAT IS A NORMAL CAT?
I believe a ‘normal cat’ to be your everyday domestic cat that is free to roam (only
during daylight hours of course!), sharing an area and being in contact with many
other cats and therefore in contact with a variety of pathogenic (disease producing)
and non-pathogenic microorganisms (bacteria, viruses, protozoans, fungi, yeast ).
Consequently, these cats are continually challenged (infected) by the local population
of microorganisms and therefore have well developed, mature immune systems
(immunocompetance). Vaccinations are helpful but do not protect cats from all
infectious diseases.
On the other hand, I believe that ‘cattery cats’ (pedigree), although vaccinated and
given lots of love and care, are maintained in isolated environments on a long term
basis are no longer ‘normal cats’. I believe there are two main reasons for this:
1. The maintenance of pedigree cats in isolated colonies (catteries) around Australia
(or any country) allows for each colony of cats to establish their own microflora
(‘normal flora’). Consequently, each colony of cats (cattery) will establish its own
epidemiological pattern. This trend also occurs in the human population. For instance,
overseas or even interstate travellers often succumb to mild to severe gastrointestinal
upsets upon relocation. These upsets are often caused by encountering a new set of
normally non-pathogenic (friendly) microorganisms that are different from the ones at
home. Cat breeders often encounter this same phenomena when a new cat is
introduced to their colony, even from a colony that is ‘just down the road’.
2. With our efforts to protect our precious and most-loved pedigree cats, I feel we
have unknowingly done them a disservice, as such isolation, not only during the
lifespan of one cat but over many generations has lead to the inability of our cats to
deal adequately with some infectious agents, including the friendly ones. They have
become immunocompromised. Again one can cite the same phenomena occurring in
the human population where a simple cold virus can have a devastating effect on a
geographically isolated group of humans eg. island populations. In fact, it is well
documented that during the colonisation of the USA, Europeans almost wiped out
entire tribes of Native Americans by introducing the measles virus.
So, where there is diminished immunocompetance associated with altered normal
microflora and/or isolation from a wide variety of pathogens, there is the potential for
altered or unusual immune responses. For instance, a microorganism that is regarded
as normal flora may now become a potential pathogen. Therefore it may be unwise
to immediately dismiss Pastuerella multocida as a possible cause of disease in some
catteries. Potentially it may be as fatal to our much loved but isolated cats as measles
was to the Native Americans!!
On the question of antibiotic use raised by the various authors, I agree with Nicholas
Jonsson that swapping from one antibiotic to another leads to the evolution of drug
resistant strains. However, it seems he failed to understand that where there is a
failure to respond to a broad spectrum antibiotic of first choice (eg penicillin
derivatives) within an acceptable time frame (and that may only be a matter of hours
in a neonatal kitten) then either the addition of (if compatible) or replacement with (if
incompatible) another antibiotic to further broaden the spectrum covered is
acceptable. This may mean introducing an antibiotic such as Antirobe to cover the
possibilities that certain bacteria regarded as ‘normal flora in normal cats’ DO produce
clinical syndromes in some ‘cattery cats’ or unusual bacteria and microorganisms that
are yet to be detected and identified (isolation, culture etc) are involved. As a
microbiologist, I quote my personal experience in this very area, where rotaviruses
(now regarded as the main cause of epidemics of gastroenteritis in humans and
animals) may still have remained undetected if we had stuck to what was regarded as
conventional thinking in the early to mid 1970's (1,2,3,4) 2. Whether we may be
research scientists, veterinarians, breeders or whatever, we MUST remain openminded when a ‘non-text book’ incident arises.
It is indeed unfortunate that research funding for small animals is so limited .... cats
are only regarded as ‘economically important’ by the people who pay their veterinary
bills!! A large portion of information on infectious disease in cats is based on what is
normal for the ‘domestic cat’, but when it comes to unusual ‘cattery cat’ problems,
much of the information is anecdotal, coming from experienced breeders. The nature
of the problem may also vary from cattery to cattery. Thus I recommend that
breeders keep detailed records of problems, symptoms, observations, living
arrangements (of the cats!!!) and even ‘gut-feelings’, as in the absence of scientific
proof, these records may be gold mines of information that avert future disasters for
themselves and other breeders.
Regards
Dr.Sue Roger-Withers, B.Sc., Ph.D.(Melb).
The personal success one breeder had had using our advised course of treatment was
neatly summed up in her letter in the same issue of the Journal:
Dear Truda,
2
References:
1. Rodger, S.M. Biochemical and biophysical characterisation of rotaviruses. 1977. Ph.D. thesis. University of Melbourne.
2. Rodger, S.M. J.A.Craven and I.Williams. 1975. Demonstration of reovirus-like particles in the intestinal contents of piglets
with diarrhoea. Aust. Vet. J.51:536.
3. Rodger, S.M. M.J.Studdert and I.H.Holmes. 1980. Characteristics of the genomes of equine rotaviruses. Vet.Microbiol.
5:243-248.
4. Rodger, S.M. R.F.Bishop, C.Birch, B.McLean and I.H.Holmes.1981. Molecular epidemiology of human rotaviruses in
Melbourne, Australia, from 1973-1979, as determined by electrophoresis of genome ribonucleic acid. J.Clin. Micro. 19:272278
I hope I'm not too late for the next RAS Journal. I have just read the Feb one at a
friends house, and I feel I simply must write and say how angry I was when I read
that vets letter about your ‘Bacteria’ series in the last two journals.
I am one of your anonymous callers, who asked you for help at the end of last year. I
had lost litters early, had mixed live and dead births, and had lost kittens early in
their lives, I was in despair. My vet had helped me a lot, but after clearing all my cats
for AIDS and leukaemia (a somewhat expensive exercise in itself), he couldn't make
any more suggestions, though in one case he did suggest that progesterone might
help during pregnancy.
After reading your first articles, I was so excited that here might be a possible
solution, that I rang my vet, and read him chunks of it over the phone. As you can
imagine, he wasn't wildly enthusiastic, but agreed to read the article, and suggested I
also talk to you. As a cautious vet, he suggested that we try the girl whose last litter
had contained one dead kitten at birth, and two more who died separately at 10 days
and 3 weeks. We used the Antirobe and Clavulox combination for 10 days from the
start of the call, and over the mating, then the repeat of 7 days Antirobe from week 5
to week 6. Five beautiful kittens, who all lived to be sold to satisfied customers. I am
now just finishing a round of litters from my other 3 Queens, all of whom had also had
some problems. While not all are yet grown to sale age, all were born live and have
thrived.
That vet's letter really angered me because the narrow attitude it displayed seemed to
suggest that no one but a vet knows anything about rearing kittens, and cat health,
and that breeders observations are worthless. He made criticisms of both you, and
implicitly your vet, and the other one who contributed, as though you were all dimwits
who needed taking down a peg.
I know that there are a lot of much happier breeders up here after this kitten season,
because you seem to have put your finger on something that has been going on - that
all are reporting 100% survivorship where they were doing poorer than 50% last
season.
I think that the time has come for some research effort to be put into discovering
whether you are really onto some new problem - as far as I can see, the fact that
Antirobe works to clear up my problem, is only a clue. My vet is also of the opinion
that your observations, and the huge response other breeders obviously made,
suggest that there is some ‘epidemic’ type problem which needs investigating.
I hope I am in time for the next journal, but I would like to remain anonymous - the
Fancy up here is very small, and not very cooperative!
Indeed we had put considerable effort into trying to isolate a causative bug, with the
co-operation of some of Sue’s colleagues, pathology tests were carried out on a
selection of kittens which had died of the apparent syndrome, using culture systems
not generally available in Veterinary Pathology labs. The final result was published in
the RASCC Journal, February 1995, and is reprinted here.
THAT BACTERIUM - ON THE TRACK AT LAST The lsolation of Group G
Streptococcus from Aborted Kittens
As promised in the November 1994 issue of the RAS Cat Control of NSW Journal, we
are able to announce that the elusive Clindamycin (Antirobe) sensitive micro-organism
that has cleverly evaded repeated attempts at isolation and identification appears to
be a Group G Streptococcus (Straede et.al. 1995).
For those owners, breeders, veterinarians and other interested persons who have
experienced or followed the saga of kitten losses due to abortion, stillbirths, foetal
abnormalities and sudden death from apparent rapid onset bronchopneumonia etc.
(RASCC journals August 1993 to November 1994, National Cat 1994) this isolation
provides relief and reassurance for all concerned. Although we had gained an insight
into treatment and control of these problems we had no idea what micro-organism(s)
were responsible for the apparent Australia-wide epidemic affecting almost all breeds
of cat.
Attempts to isolate and identify a Clindamycin-sensitive micro-organism have been
hampered by a number of factors related to the nature of the Group G Streptococci
and the pattern of disease. The nature of the bacterium is such that it can easily
remain undetected by routine Laboratory testing. In relation to the pattern of disease,
problems experienced by breeders resemble patterns that are consistent with other
diseases such as feline leukaemia, feline immunodeficiency virus (cat AIDS),
Chlamydia or mycoplasma. Frustration among
breeders arose when extensive
laboratory testing and retesting as well as aggressive antibiotic treatment programs
for such micro-organisms proved unsuccessful.
Following successful treatment of the symptoms and pattern of disease with
Clindamycin, the authors began searching for another cause. With the help of the
Victorian Department of Agriculture as well as frustrated breeders and veterinarians
from all over Australia who were willing to provide specimens, Group G Streptococci
were first isolated from stillborn kittens obtained from a Western Australian breeder.
After following a treatment program outlined by the authors, there has been no
recurrence of the problem in this cattery. It is interesting to note that while group G
Streptococci have been associated with sinusitis, septicaemia and endocarditis in
humans (Review Medical Microbiology 18thEd), the only recorded isolation of Group G
Streptococci in cats was in association with infectious lymphadenitis (Swindle et al.
1980). Also, in humans, Clindamycin is indicated for serious infections of the
respiratory tract and infections of the female pelvis and genital tract (endometritis,
ovarian abscesses, pelvic cellulitis, vaginal cuff infections) that are caused by
Streptococci able to survive with little oxygen (including Group G) (Mims Annual
1994). It appears that the patterns of disease in humans closely resemble those
patterns observed by cat breeders. It is now necessary to conduct further research to
establish the role of the Group G Streptococci in breeding losses in cats.
During routine laboratory testing for possible causative agents, a number of other
bacteria have also been occasionally isolated. These include Pastuerella multocida
some untyped Streptococci (which may have included Group G) and a * Gram positive
bacillus that to date is unable to be identified. The significance of such isolates is yet
to be established, but supports the authors’ view that well conducted research now be
performed to resolve a potentially complex issue regarding feline reproductive
disorders.
The possibility that a number of other causative agents may exist is further supported
by the observation that the described pattern of reproductive and/or respiratory
problems can sometimes be resolved with antibiotics other than Clindamycin. These
include lincomycin (related to Clindamycin) and tetracyclines. Although these
observations may be explained by variations in drug sensitivity, it does raise another
very important aspect to problem management: the choice of antibiotic must be
based on bacterial drug sensitivity testing.
Until recently, Antirobe (Clindamycin) was not scheduled for use in cats. However,
due to its increasing widespread use throughout Australia by cat breeders it has now
been scheduled. While many breeders have successfully eliminated their breeding
and/or kitten problems with Clindamycin, it is very important that Clindamycin does
not become the ‘magic bullet’ and be used indiscriminately for everything. It has been
reported that some bacteria rapidly develop resistance to Clindamycin (Mims Annual
1994) and as responsible breeders, the last thing we need is to create Clindamycin
*Gram= Gram stain - a basic laboratory test used in preliminary identification of bacteria.
resistant bacteria through misuse and abuse of the antibiotic!!! It is now more
important than ever that, where possible, antibiotic selection be based on the results
of drug sensitivity testing. Now that we are progressing with the detection of
causative agents, veterinary diagnostic laboratories will be able to perform tests to
help select the correct antibiotic. If antibiotics are used incorrectly or inappropriately,
then a breeder in distress may risk further disasters eg. queens becoming carriers and
at times of stress (during pregnancy, travel etc) shedding the organisms to other
queens or perhaps experiencing a recurrence of the problem themselves.
Anyone who may be experiencing repeated breeding and/or kitten losses similar to
the described pattern, and even if only trouble-some, is encouraged to have samples
tested. Once the correct bacterial sensitivity has been determined, the results have
been spectacular. There is improved reproductive success, minimal kitten losses
(abortions, deformities, respiratory infections) and consequently, reduced veterinary
costs, not to mention reduced stress for the owners!!!!
Breeders are encouraged to contact the authors before launching into testing and/or
treatment programs blindfold. Advice is available regarding testing (now relatively
simple and inexpensive) and treatment strategies. Should you so wish, your
confidentiality will be respected.
In summary, the isolation of Group G Streptococci associated with breeding problems
in cats is a major step forward (and a relief to many) in understanding and controlling
what appears to be a nation wide epidemic. There is still a way to go in obtaining ‘the
real story’ but with the help of willing and responsible breeders and the co-operation
of veterinarians and veterinary laboratories, we can jointly put the puzzle together.
The Authors:
Dr T M Straede B.Sc. Ph.D. Nintu Cattery NSW (02)4575 0227
Dr S M Rodger-Withers BSc DAc PhD Member Australian Society of Microbiology,
Member Victorian Society of Venereology FCCV Qihai Cattery Victoria (03)9391 5028
Dr Karen Hedberg B.V.Sc North Richmond Veterinary Hospital NSW (02) 4571 2042
Jeanette Perkins B.S.W ,C.O.A.WA. Satu Cattery Western Australia (08) 9821 2171
The authors wish to thank breeders, veterinarians and all interested persons who have
provided specimens, encouragement help and support in getting this project off the
ground.
References
Swindle M M and Norayan 0 1980. Contagious Streptococcal lymphadenitis in cats.
J.A.V.M.A. 177 829-830
In conclusion I would like to say that whether or not there is indeed a complete
syndrome as suggested in my original hypothesis, the value of the use of Clindamycin
(Antirobe) has been further investigated, particularly by Dr Richard Malik (Veterinary
Science, Sydney University), in relation to its use in treating upper respiratory
infections in cats.
This appendix is very much a ‘work in progress’. Even if it never again provides a
specific answer to a breeder’s problem, it may demonstrate that breeders are able to
pursue their own elusive feline health problem, ‘with a little help from their vets, and
‘friends’.