|
1. Feline Cryptococcosis
2. Rabies 3. Nasitrema migrans 4. Rat abscess |
|
Feline Cryptococcosis:
History and Clinical Description: The following 3 images are taken from a cat with a 4-6 week history of progressive hind limb ataxia, decreased activity and weight loss. Ataxia progressed to collapsing in rear and crossing over in font. On presentation the cat was obtunded with generalized ataxia, and was dehydrated. On exam there was decreased conscious proprioception in all four limbs. Hopping response was dragging to unresponsive in the right and dragging to slow on the left. Right head turn, walked in tight circles to the right. Anisocoria: present OD larger than OS. Vertical, horizontal, and positional nystagmus. An MRI showed a hyperintense area on T2 left frontal lobe. Also a few lesions on the left cerebrum. Diagnosis: Multifocal brain disease.
More often associated with warm, humid climates, this case of infection with Cryptococcus neoformans was submitted from Wisconsin, USA. Avian, particullarly pigeon droppings are common sources of infection, and as with most fungal infections, immunosuppression often allows infection with this common yeast. Round bodies surrounded by a clear capsule are evident in the H&E stained image, giving the classically decsribed "soap bubble" appearence. Capsules will stain strongly positive with PAS or mucicarmine stains.
More often associated with warm, humid climates, this case of infection with Cryptococcus neoformans was submitted from Wisconsin, USA. Avian, particullarly pigeon droppings are common sources of infection, and as with most fungal infections, immunosuppression often allows infection with this common yeast. Round bodies surrounded by a clear capsule are evident in the H&E stained image, giving the classically decsribed "soap bubble" appearence. Capsules will stain strongly positive with PAS or mucicarmine stains.
Rabies
General information on rabies can be found under Society and Infectious Disease, Rabies page on this web site.
A 3 year old Quarter horse mare stabled at a breeding facility in Kentucky, USA presented with rapidly progressing neurologic signs over a 4 day period. The horse was normal prior to presentation and had been annually vaccinated for EEE, WEE and tetanus. On the first day the horse was reported to have gone off feed and was dull and depressed. The horse became hypersensitive to touch, was seen gnawing at its flank and legs, and rapidly progressed to convulsions once these behavioral changes were noted. On the fourth day the horse became recumbent and died.
Differentials for the clinical presentation in this horse could also include: tetanus, equine herpes, moldy corn poisoning, lead toxicity, and other causes of encephalitis (EEE,WEE,VEE)
Histologic lesions: Non-suppurative polioencephalomyelitis with craniospinal ganglionitis. Inflammation is most severe in the brainstem, but tends to be limited in relation to the amount of virus present. Neuronal necrosis, neuronophagia, lymphocytic perivascular cuffing, microgliosis, and later astrogliosis also occur . Well deliniated round or oval, eosinophilic inclusions located in the cytoplasm of neurons are called Negri bodies; and they may be found in otherwise normal appearing neurons anywhere, but in ruminants are more often found in the cerebellar Purkinje cells, and in carnivores in hippocampal neurons. In skunks and foxes a spongiform change (vacuolation of gray matter neuropil) similar to scrapie may develop.
A 3 year old Quarter horse mare stabled at a breeding facility in Kentucky, USA presented with rapidly progressing neurologic signs over a 4 day period. The horse was normal prior to presentation and had been annually vaccinated for EEE, WEE and tetanus. On the first day the horse was reported to have gone off feed and was dull and depressed. The horse became hypersensitive to touch, was seen gnawing at its flank and legs, and rapidly progressed to convulsions once these behavioral changes were noted. On the fourth day the horse became recumbent and died.
Differentials for the clinical presentation in this horse could also include: tetanus, equine herpes, moldy corn poisoning, lead toxicity, and other causes of encephalitis (EEE,WEE,VEE)
Histologic lesions: Non-suppurative polioencephalomyelitis with craniospinal ganglionitis. Inflammation is most severe in the brainstem, but tends to be limited in relation to the amount of virus present. Neuronal necrosis, neuronophagia, lymphocytic perivascular cuffing, microgliosis, and later astrogliosis also occur . Well deliniated round or oval, eosinophilic inclusions located in the cytoplasm of neurons are called Negri bodies; and they may be found in otherwise normal appearing neurons anywhere, but in ruminants are more often found in the cerebellar Purkinje cells, and in carnivores in hippocampal neurons. In skunks and foxes a spongiform change (vacuolation of gray matter neuropil) similar to scrapie may develop.
Nasitrema migrans
Clinical History: Images presented below are from an adult female Atlantic Bottlenose dolphin (Tursiops truncatus) found stranded on Assateaque Island on September 6, 1999. Physical exam revealed numerous healing skin lacerations located on the flukes, dorsum, and lateral body wall, suggestive of a shark attack in recent days to weeks. A focally extensive ulcerative dermatitis was located over the rostrum and peduncles. The animal was transported to the National Aquarium in Baltimore where she was treated for approximately five weeks. Her clinical course included a moderate to severe regenerative anemia, a non-healing ulcerative dermatitis, and a lymphopenia with rising eosinophilia. In spite of an excellent appetite and weight gain, the dolphin was seen suddenly struggling to breath on the evening of October 15,1999. Following this brief episode of apnea, she rolled over and sank to the bottom of the tank.
Necropsy Findings:
Significant lesions found in the general necropsy included moderate focally extensive myocardial necrosis, lymphadenopathy, and granulomas in the lungs, stomach, spleen, lymph nodes and pancreas. Grossly, the brain showed an area of adherent, thickened meninges located along the ventral surface of the brainstem at the level of the left vestibulocochlear cranial nerve.
Histologic findings:
There is a locally extensive lymphoplasmacytic and granulomatous meningitis associated with the base of the pons and the area of the left eighth cranial nerve. Within the meninges are numerous refractile brown-yellow triangular parasite eggs, which range from 50 to 70 microns in diameter. Most of the parasite eggs are not viable, but a few are embryonated. Multi-nucleate giant cells surround many of the ova. Extending into the brain parenchyma are multiple necrotic tracts with associated edema, mild gliosis, and intralesional parasite eggs. There is a mild to moderate multifocal perivascular lymphoplasmacytosis. No adult parasites were found in the brain.
Diagnosis: Lymphoplasmacytic meningoencephalitis secondary to trematode (Nasitrema sp.) parasite migration.
References:
Morimitsu, T., et al. (1987) Mass Stranding of Odontoceti Caused by Parasitogenic Eighth Cranial Neuropathy. J Wildl Dis 23(4):586-590.
Lewis, R.J. and Berry, K. (1988) Brain Lesions in a Pacific White-sided Dolphin (Lagenorhynchus obliquidens). J Wildl Dis 24(3):577-581.
O’Shea, T.J., et al. (1991) Nasitrema sp.-associated Encephalitis in a Striped Dolphin (Stenrlla coeruleoalba) Stranded in the Gulf of Mexico. J Wildl Dis 27(4):706-709.
READ MORE about this and other infectious diseases in dolphins on this site.
Necropsy Findings:
Significant lesions found in the general necropsy included moderate focally extensive myocardial necrosis, lymphadenopathy, and granulomas in the lungs, stomach, spleen, lymph nodes and pancreas. Grossly, the brain showed an area of adherent, thickened meninges located along the ventral surface of the brainstem at the level of the left vestibulocochlear cranial nerve.
Histologic findings:
There is a locally extensive lymphoplasmacytic and granulomatous meningitis associated with the base of the pons and the area of the left eighth cranial nerve. Within the meninges are numerous refractile brown-yellow triangular parasite eggs, which range from 50 to 70 microns in diameter. Most of the parasite eggs are not viable, but a few are embryonated. Multi-nucleate giant cells surround many of the ova. Extending into the brain parenchyma are multiple necrotic tracts with associated edema, mild gliosis, and intralesional parasite eggs. There is a mild to moderate multifocal perivascular lymphoplasmacytosis. No adult parasites were found in the brain.
Diagnosis: Lymphoplasmacytic meningoencephalitis secondary to trematode (Nasitrema sp.) parasite migration.
References:
Morimitsu, T., et al. (1987) Mass Stranding of Odontoceti Caused by Parasitogenic Eighth Cranial Neuropathy. J Wildl Dis 23(4):586-590.
Lewis, R.J. and Berry, K. (1988) Brain Lesions in a Pacific White-sided Dolphin (Lagenorhynchus obliquidens). J Wildl Dis 24(3):577-581.
O’Shea, T.J., et al. (1991) Nasitrema sp.-associated Encephalitis in a Striped Dolphin (Stenrlla coeruleoalba) Stranded in the Gulf of Mexico. J Wildl Dis 27(4):706-709.
READ MORE about this and other infectious diseases in dolphins on this site.
Brain abscess.
These images are from a 2 month old female rat. Her main presenting sign was poor condition since birth; her siblings were reported to be fit and well. She was treated with antibiotics for a respiratory infection 2 weeks prior to presenting with circling to the left constantly, ataxia and nystagmus. She also had snuffly breathing and dried blood on her nose.
Brain: Extending from the left meninges into the cerebellar white and grey matter is a locally extensive area of abscessation. Centrally composed of degenerate neutrophils, the wall of the abscess includes neutrophils, lymphocytes, and a dense population of plasma cells. Tissue around the described area includes neovascularization with perivascular plasmacytic cuffing and gliosis. Gram staining did not reveal bacteria within or around the large abscess.
Interestingly, there were also multiple foci of chronic inflammation scattered within rostral to mid-cortical cerebral hemispheres. These foci include macrophages and microglia surrounding abundant gram- positive bacteria.
Brain; left cerebellum and associated meninges: Abscess.
Brain; cerebral hemispheres: Moderate, multifocal, non-suppurative encephalitis with intralesional gram-positive bacteria.
There was a large brain abscess on the left side of the cerebellum that caused the described neurologic signs. The brain/meninges may have been seeded at the time of the described respiratory infection; prominent BALT and lymphoplasmacytic cuffing seen around blood vessels in the lungs is suggestive of Mycoplasma sp. infection, but consolidation consistent with active pneumonia was not found. The abscess was not cultured, so the etiology is not known. While Staphylococci or Streptococcus are likely candidates for the bacteria identified on gram stain, the distribution of bacteria and the inflammatory response in the two locations in the brain does not make sense to me; I was surprised to not see any gram positive bacteria in the abscess and wonder if there was a different bacterium that caused it.
You can CLICK HERE to read about Citrobacter koseri , a gram negative bacterium know to cause brain abscesses in neonatal humans, and found to make similar lesions in rat models.
Brain: Extending from the left meninges into the cerebellar white and grey matter is a locally extensive area of abscessation. Centrally composed of degenerate neutrophils, the wall of the abscess includes neutrophils, lymphocytes, and a dense population of plasma cells. Tissue around the described area includes neovascularization with perivascular plasmacytic cuffing and gliosis. Gram staining did not reveal bacteria within or around the large abscess.
Interestingly, there were also multiple foci of chronic inflammation scattered within rostral to mid-cortical cerebral hemispheres. These foci include macrophages and microglia surrounding abundant gram- positive bacteria.
Brain; left cerebellum and associated meninges: Abscess.
Brain; cerebral hemispheres: Moderate, multifocal, non-suppurative encephalitis with intralesional gram-positive bacteria.
There was a large brain abscess on the left side of the cerebellum that caused the described neurologic signs. The brain/meninges may have been seeded at the time of the described respiratory infection; prominent BALT and lymphoplasmacytic cuffing seen around blood vessels in the lungs is suggestive of Mycoplasma sp. infection, but consolidation consistent with active pneumonia was not found. The abscess was not cultured, so the etiology is not known. While Staphylococci or Streptococcus are likely candidates for the bacteria identified on gram stain, the distribution of bacteria and the inflammatory response in the two locations in the brain does not make sense to me; I was surprised to not see any gram positive bacteria in the abscess and wonder if there was a different bacterium that caused it.
You can CLICK HERE to read about Citrobacter koseri , a gram negative bacterium know to cause brain abscesses in neonatal humans, and found to make similar lesions in rat models.
