scholarly journals A PARALYTIC DISEASE OF GUINEA PIGS DUE TO THE TUBERCLE BACILLUS

1929 ◽  
Vol 50 (3) ◽  
pp. 365-370 ◽  
Author(s):  
Richard E. Shope ◽  
Paul A. Lewis
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tuberculous Meningitis ◽  
Guinea Pigs ◽  
Tuberculous Infection ◽  
Tubercle Bacillus ◽  
Herpes Encephalitis ◽  
Subsequent Publication ◽  
The Central Nervous System ◽  
Rule Out

The experimental data collected during this study of a transmissible type of paralysis developing in tuberculous guinea pigs indicate the condition to be a true tuberculous meningitis. We have been able to rule out the possibility that it is due to a non-tuberculous infection of the central nervous system caused by Roemer's virus, or by an atypical herpes virus, or by some bacterium other than the tubercle bacillus. Roemer's virus and herpes could be eliminated from consideration when Berkefeld N filtrates of infectious brain emulsions proved incapable of reproducing the disease. Furthermore, rabbits could be infected as they cannot with Roemer's virus, and the disease elicited in rabbits bears no semblance to herpes encephalitis. No organism other than the tubercle bacillus could be obtained on culturing brain or brain emulsions from experimental cases, and no others were seen in examining fresh smear preparations from the central nervous system. In a modified Noguchi medium a tubercle bacillus possessing atypical staining properties was obtained. This organism was capable of producing the typical paralytic disease when injected intracerebrally into guinea pigs, and also generalized tuberculosis in animals inoculated subcutaneously with it. Typical tuberde bacilli were readily demonstrable in sections of the meninges from animals with the disease, and culture of pieces of brain on Dorset's egg medium usually yielded a growth of tubercle bacilli. Only in the first of the experimental passages, on the other hand, was it possible to demonstrate acid-fast organisms in fresh smear preparations from the central nervous system. This fact and the attributes of the atypically staining organisms encountered in the cultures in Noguchi media will be considered more fully in a subsequent publication. In view of the much discussed question of the filtrability of the tubercle bacillus our observations concerning the failure of this organism to pass a Berkefeld N filter are of interest. No animal in our series inoculated intracerebrally with brain emulsion from either a "spontaneous" or experimental case of tuberculous meningitis failed to develop meningitis, and that rather acutely, while no animal in our series injected with a Berkefeld filtrate of brain emulsion has developed tuberculous meningitis or any other form of tuberculosis. In connection with this observation it must be recalled that the organism was atypical in respect to its staining qualities at least.

Central nervous system control of airway tone in guinea pigs: the role of histamine

1988 ◽  
Vol 65 (5) ◽  
pp. 2024-2029 ◽  
Author(s):  
P. J. Mauser ◽  
N. H. Edelman ◽  
R. W. Chapman
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pigs ◽  
Lung Compliance ◽  
System Control ◽  
The Central Nervous System ◽  
Dose Dependent Decrease ◽  
Airway Tone ◽  
Dynamic Lung Compliance ◽  
H1 Antagonist

The central nervous system (CNS) plays an important role in the reflex control of bronchomotor tone, but the relevant neurotransmitters and neuromodulators have not been identified. In this study we have investigated the effect of histamine. Anesthetized male guinea pigs were prepared with a chronically implanted intracerebroventricular (icv) cannula and instrumented for the measurement of pulmonary resistance (RL), dynamic lung compliance (Cdyn), tidal volume (VT), respiratory rate (f), blood pressure (BP), and heart rate (HR). Administration of histamine (2-30 micrograms) icv caused a significant (P less than 0.05) reduction of Cdyn with no change in RL, VT, and f. At a dose of 100 micrograms icv, histamine caused an increase in RL (202 +/- 78%), a reduction of Cdyn (77 +/- 9%), an increase in f (181 +/- 64%), and a reduction of VT (53 +/- 18%). There were no changes in BP and HR after 100 micrograms of icv histamine. In contrast, intravenous administration of histamine (0.1-2 micrograms/kg) caused a dose-dependent decrease in Cdyn and increase in RL that was associated with tachypnea at each bronchoconstrictor dose. Intravenous histamine (2 micrograms/kg) produced a fall in BP and an increase in HR. The bronchoconstrictor responses to icv histamine were completely blocked by vagotomy and significantly reduced by atropine (0.1 mg/kg iv), whereas vagotomy and atropine did not block the bronchospasm due to intravenous histamine. Additional studies indicated that the pulmonary responses due to icv histamine (100 micrograms) were blocked by pretreatment with the H1-antagonist chlorpheniramine (1 and 10 micrograms, icv). These data indicate that histamine may serve a CNS neurotransmitter function in reflex bronchoconstriction in guinea pigs.

Neonatal stridor in association with herpes simplex infection of the larynx

1998 ◽  
Vol 112 (12) ◽  
pp. 1192-1193 ◽  
Author(s):  
H. R. Sharp ◽  
S. P. A. Blaney ◽  
G. A. J. Morrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Herpes Simplex ◽  
Neonatal Period ◽  
Upper Aerodigestive Tract ◽  
Herpes Encephalitis ◽  
Simplex Infection ◽  
The Central Nervous System ◽  
Localized Disease ◽  
Simplex Virus

AbstractHerpes simplex virus (HSV) infection in the neonatal period may be confined to the eyes, skin and upper aerodigestive tract or may be widely disseminated to other organs, with particular recognition of involvement of the central nervous system (CNS) causing herpes encephalitis (Whitley et al., 1980a, b; Andersen, 1987).Primary laryngeal HSV infection is extremely uncommon. We present a case of acute neonatal stridor secondary to such localized disease and discuss its management.

scholarly journals INDUCED RESISTANCE OF THE CENTRAL NERVOUS SYSTEM TO EXPERIMENTAL INFECTION WITH EQUINE ENCEPHALOMYELITIS VIRUS

1944 ◽  
Vol 80 (3) ◽  
pp. 197-211 ◽  
Author(s):  
R. Walter Schlesinger ◽  
Peter K. Olitsky ◽  
Isabel M. Morgan
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pigs ◽  
Early Stage ◽  
Neutralizing Antibody ◽  
Challenge Dose ◽  
Abortive Infection ◽  
Encephalomyelitis Virus ◽  
The Central Nervous System ◽  
Western Equine Encephalomyelitis Virus

Although vaccination of guinea pigs with formalin-inactivated Western equine encephalomyelitis virus rendered them specifically immune to an intracerebral challenge dose of 1,000 M.L.D. of Western virus, it failed to protect their central nervous system against the initial effects of the virus: the intracerebral challenge dose was followed by an abortive infection of 20 to 30 hours' duration characterized by fever and histopathological changes which simulated the response at that early stage of non-vaccinated control animals. During the abortive infection of immune animals, virus could occasionally be demonstrated in their brains; indeed, it was detected with about the same frequency it was isolated from brains of similarly inoculated, non-immune guinea pigs during corresponding early phases of the infection. About one week after the abortive infection there was found a marked transitory accumulation of specific neutralizing antibody in the brain tissue. See PDF for Equation equalled at this time 1:1 to 1:10 instead of the value of about 1:300 found under physiological conditions. Guinea pigs which had recovered from an abortive infection with Western virus were resistant for a limited period of time to the effects of intracerebral inoculations of the immunologically distinct viruses of Eastern equine encephalomyelitis or vesicular stomatitis.

scholarly journals LETHAL CARDIAC ANAPHYLAXIS IN THE RABBIT

1911 ◽  
Vol 14 (5) ◽  
pp. 476-496 ◽  
Author(s):  
J. Auer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Right Ventricle ◽  
Guinea Pigs ◽  
Harmful Effect ◽  
Finger Nail ◽  
The Central Nervous System ◽  
Intact Rabbit ◽  
The Right ◽  
Lethal Anaphylaxis

Acute lethal anaphylaxis in the intact rabbit is caused by a failure of the heart. This failure of the heart is due to a change in the heart itself; it is peripheral and independent of the central nervous system for its production. This change in the heart is shown anatomically and functionally by decreased translucency, change in consistency, and by failure to respond to stimuli, and is probably to be classed as a chemical rigor. The rigor of the heart is most pronounced in the right ventricle, the wall of which may be gray, stiff, very tough to the finger nail, and non-irritable. Cardiac stimulants of the digitalis group seem to exert a harmful effect when injected in acute anaphylaxis. Blood coagulation is delayed; a loose clot forms after one half to two hours. Anti-anaphylaxis is produced when the animal does not succumb to the injection. When anaphylactic death is delayed for about one hour, a well developed rigor of the white muscles of the thigh, and of the diaphragm may occur while the animal is still alive. Reasons are brought forward to show the necessity of more caution in employing the word anaphylaxis. Friedberger's statement, that the lungs of guinea pigs dead from acute anaphylaxis are not characteristic of anaphylaxis for this animal, is shown to be baseless.

scholarly journals STUDIES IN RODENT POLIOMYELITIS

1942 ◽  
Vol 76 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Claus W. Jungeblut ◽  
Rose R. Feiner ◽  
Murray Sanders
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Flaccid Paralysis ◽  
Nerve Tissue ◽  
Subcutaneous Route ◽  
Poliomyelitis Virus ◽  
The Central Nervous System

1. Murine SK poliomyelitis virus has been transferred from mouse to guinea pig with the establishment of a fixed strain of cavian passage virus. 2. The disease thus produced in guinea pigs is characterized by the occurrence of flaccid paralysis. Typical poliomyelitic lesions are found in the anterior horn of the spinal cord. 3. Guinea pigs are susceptible to infection with murine virus by the intracerebral, intravenous, intraperitoneal, and subcutaneous route; cavian passage virus produces paralysis only upon intracerebral or intravenous injection. Neither virus paralyzes guinea pigs by feeding or nasal instillation. 4. The potency of the virus (murine or cavian) in guinea pigs is considerably lower than in mice and compares with the titer of the original SK strain in monkeys. In paralyzed guinea pigs the virus is found only in the central nervous system and not in extraneural sites, such as blood or abdominal viscera. 5. Attempts to cultivate cavian passage virus in tissue culture have yielded evidence of some in vitro propagation but no passage virus has as yet been obtained by this method. 6. Cross neutralization tests with cavian passage virus in guinea pigs and with murine virus in mice have established the serological identity of the two viruses. Inactivation of cavian passage virus in guinea pigs by poliomyelitis-convalescent monkey sera is irregular. Complete neutralization has been obtained with a concentrated poliomyelitis horse serum. 7. Resistance to reinfection with potent virus can be demonstrated in convalescent guinea pigs as well as in guinea pigs which have survived a symptomless infection with either murine or cavian virus. This immunity is demonstrable by the power of the serum of such animals to neutralize the virus in vitro and by the ability of nerve tissue to dispose in vivo of the infectious agent. 8. Cavian passage virus has a limited pathogenicity for rhesus monkeys. Of a total of 35 monkeys injected intracerebrally with guinea pig passage virus 26 failed to respond with any manifest symptoms of disease; 8 monkeys showed various signs of definite involvement of the central nervous system consisting of tremor, convulsions, facial palsy, and localized pareses; 1 monkey developed typical flaccid paralysis. 9. Following injection with cavian virus the virus may be recovered from the tissues of normal monkeys but not from the tissues of convalescent monkeys shortly after a paralyzing attack of poliomyelitis due to SK or Aycock virus. 10. Immunization of monkeys with early cavian passage virus by the subcutaneous route has given no clear-cut evidence of protection against intracerebral reinfection with SK poliomyelitis virus. Neither has there been any evidence of effective interference in monkeys injected intravenously with early cavian passage virus and intracerebrally with RMV poliomyelitis virus. 11. The bearing of the experimental data upon the epidemiology of the human disease is discussed.

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